Apoptosis Cancer Research Results
Apoptosis, Apoptosis: Click to Expand ⟱
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| Type: type of cell death |
Situation in which a cell actively pursues a course toward death upon receiving certain stimuli.
Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die.
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Scientific Papers found: Click to Expand⟱
TumCD↑, Hyperthermic temperatures (41.8 or 43°C) enhanced significantly trabectedin-related clonogenic cell death and G2/M cell cycle arrest followed by cell type-dependent induction of apoptosis or senescence.
TumCCA↑,
Apoptosis↑,
BRCA2↓, Expression of BRCA2 protein, an integral protein of the HRR machinery, was significantly decreased by heat.
ChemoSen↑, The findings establish BRCA2 degradation by heat as a key factor for a novel treatment strategy that allows targeted chemosensitization to tra
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Review, |
AD, |
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Review, |
Var, |
NA |
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*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2/PTGS2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE/β-secretase↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.
TumCG↓, suppression growth by 1,8-cineole in the leukemia cell lines results from the induction of apoptosis by this compound.
selectivity↑, In contrast, we observed no induction of apoptosis by 7.5 to 15 |iM 1,8-cineole in normal lymphocytes prepared from healthy volunteers
Apoptosis↑, 1,8-cineole might exert its antitumor activity by triggering apoptosis in human leukemia cells
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in-vitro, |
Melanoma, |
A431 |
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in-vitro, |
OS, |
MG63 |
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in-vitro, |
Nor, |
HaCaT |
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TumCP↓, HE has showed increased anti-proliferative effect against the cancer cells but was resisted by non-malignant cells.
selectivity↑,
AntiCan↑, 1,8-Cineole has shown potential anti-cancer activity in a dose-dependent manner, and cell death was induced through ROS-mediated apoptosis.
TumCD↑,
Apoptosis↑,
Dose↝, 10 mg mL-1 concentration was able to cause >45% cell death in A431 and >20% in MG-63, as against only about 6% in HaCaT cells.
ROS↑, HE-C increased ROS production in cancer cells
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vitro+vivo, |
Colon, |
HCT116 |
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TumCP↓, anti-proliferative effect of 1, 8-cineole on human colon cancer cell lines HCT116 and RKO by WST-8 and BrdU assays.
Apoptosis↑, Specific induction of apoptosis, not necrosis, was observed in human colon cancer cell lines HCT116 and RKO by 1, 8-cineole.
survivin↓, 1, 8-cineole was associated with inactivation of survivin and Akt and activation of p38.
Akt↓,
p38↑,
cl‑PARP↑, induced cleaved PARP and caspase-3, finally causing apoptosis.
cl‑Casp3↑,
TumVol↓, 1, 8-cineole inhibits tumor growth of RKO xenografts.
Glycolysis↓, 2-DG inhibits glycolysis due to formation and intracellular accumulation of 2-deoxy-d-glucose-6-phosphate (2-DG6P), inhibiting the function of hexokinase and glucose-6-phosphate isomerase, and inducing cell death
HK2↓,
mt-ROS↑, 2-DG-mediated glucose deprivation stimulates reactive oxygen species (ROS) production in mitochondria, also leading to AMPK activation and autophagy stimulation.
AMPK↑,
PPP↓, 2-DG has been shown to block the pentose phosphate shunt
NADPH↓, Decreased levels of NADPH correlate with reduced glutathione levels, one of the major cellular antioxidants.
GSH↓,
Bax:Bcl2↑, Valera et al. also observed that in bladder cancer cells, 2-DG treatment modulates the Bcl-2/Bax protein ratio, driving apoptosis induction
Apoptosis↑,
RadioS↑, 2-DG radiosensitization results from its effect on thiol metabolism
eff↓, (NAC) treatment, downregulated glutamate cysteine ligase activity, or overexpression of ROS scavenging enzymes
Half-Life↓, its plasma half-life was only 48 min [117]) make 2-DG a rather poor drug candidate
other↝, Adverse effects of 2-DG administration in humans include fatigue, sweating, dizziness, and nausea, mimicking the symptoms of hypoglycemia
eff↓, Moreover, 2-DG has to be used at relatively high concentrations (≥5 mmol/L) in order to compete with blood glucose
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in-vitro, |
Lung, |
H23 |
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in-vitro, |
Lung, |
KP2 |
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in-vivo, |
NA, |
NA |
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HK2↓, 2-DG, an inhibitor of HK2, inhibited human and mouse lung cancer cell growth through inducing cell apoptosis and autophagy.
Apoptosis↑,
TumAuto↑,
TumCG↓, these studies showed that the 2-DG, HK2 inhibitor, suppresses lung cancer cell growth in vivo.
tumCV↓, ISO reduced the survival rate of gastric cancer AGS cells, but the toxicity to normal cells was minimal. Isoorientin Reduces the Viabilities of Gastric Cancer Cells
selectivity↑,
*toxicity↓,
Apoptosis↑, ISO induced apoptosis in gastric cancer AGS cells
ROS↑, level of reactive oxygen species (ROS) in gastric cancer AGS cells also increased with the extension of the ISO treatment time
eff↓, However, cell apoptosis was inhibited by preconditioning cells with N–acetylcysteine (NAC).
TumCCA↑, ISO arrested the cell cycle at the G2/M phase by increasing intracellular ROS levels.
p‑Akt↓, ISO inhibited cell migration by inhibiting the expression of p–AKT, p–GSK–3β, and β–catenin and was also related to the accumulation of ROS.
p‑GSK‐3β↓,
β-catenin/ZEB1↓,
TumCMig↓, Isoorientin Inhibited AGS Cell Migration via the AKT/GSK–3β/β–catenin Signaling Pathways
Twist↓, Twist, ZEB1, N–cadherin, and β–catenin were all decreased, while the expression levels of E-cadherin were increased
N-cadherin↑,
β-catenin/ZEB1↓,
E-cadherin↑,
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in-vitro, |
CRC, |
DLD1 |
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NA, |
NA, |
HCT116 |
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eff↑, Our results demonstrated that the co-treatment of 3-BP and cetuximab synergistically induced an antiproliferative effect in both CRC cell lines
Ferroptosis↓, co-treatment induced ferroptosis, autophagy, and apoptosis.
TumAuto↑,
Apoptosis↑,
FOXO3↑, co-treatment inhibited FOXO3a phosphorylation and degradation and activated the FOXO3a/AMPKα/pBeclin1 and FOXO3a/PUMA pathways, leading to the promotion of ferroptosis, autophagy, and apoptosis in DLD-1
AMPKα↑,
p‑Beclin-1/ATG6↑,
HK2↓, 3-Bromopyruvate (3-BP), also known as hexokinase II inhibitor II, has shown promise as an anticancer agent against various types of cancer
ATP↓, 3-BP exerts its anticancer effects by manipulating cell energy metabolism and regulating oxidative stress, as evidenced by the accumulation of reactive oxygen species (ROS) [13,14,15,16].
ROS↑,
Dose↝, Eight days postinoculation, xenografted mice were randomly divided into four groups and intraperitoneally injected with PBS, 3-BP, cetuximab, or a combination of 3-BP and cetuximab every four days for five injections.
TumVol↓, 3-BP alone or co-treatment with 3-BP and cetuximab significantly reduced the tumor volume and tumor weight on Day 28, but co-treatment showed a greater reduction than 3-BP alone
TumW↓,
xCT/SLC7A11↑, The protein level of SLC7A11 was significantly upregulated in all three cell lines following co-treatment (Fig. 2B).
GSH↓, co-treatment with 3-BP and cetuximab led to glutathione (GSH) depletion (Fig. 2D), reactive oxygen species (ROS) production
eff↓, Knockdown of either ATG5 or Beclin1 attenuated the cell death and MDA production induced by co-treatment
MDA↑,
toxicity↑, 3-Bromopyruvate (3BP), a small alkylating
agent, acts as an anti-metabolite to vital substrates in cancer metabolism and exhibits antitumor activity
across various cancer types, but the unformulated 3BP can cause high toxicity
eff↝, This study explores the efficacy of the 3BP clinical derivative KAT/3BP, currently in phase 1 for patients with hepatocellular carcinoma, in lymphoma models.
eff↑, AT/3BP exhibited synergistic activity when combined with lymphoma therapies, including bendamustine and R-CHOP.
Glycolysis↓, At acidic extracellular pH, 3BP enters cancer cells via monocarboxylic acid-1 (MCT-1) and inhibits glycolysis
through hexokinase II (HK-2) covalent modification
HK2↓, with HK-2 inhibition and dissociation from mitochondria, apoptosis-inducing factor (AIF) release, and apoptosis induction (9).
AIF↑,
Apoptosis↑,
NK cell↑, In the latter, tumor growth was in vivo reversed, with an increase in the number of circulating CD4+, CD8+, and NK-
cells
toxicity↑, unformulated 3BP administrations are associated with severe toxicities, including deaths (22,23)
toxicity↓, However, improvements have been made in developing novel 3BP formulations based on
liposomes, polyethylene glycol (PEG), PEGylated liposomes (stealth liposomes), perillyl alcohol
formulations, and others (12,22,24
Dose↝, KAT-101 and KAT-201 are two clinical 3BP derivatives formulated for oral or intratumoral (IT) administration, respectively (National Cancer Institute Thesaurus Codes C193479 and
C193479), now entering the early clinical evaluation of patients with h
AntiTum↑, KAT/3BP has in vivo antitumor activity in a syngeneic mouse model.
Glycolysis↓, Under acidic extracellular pH, 3BP is transported into cancer cells via monocarboxylate transporter 1 (MCT1), inhibiting glycolysis by covalently modifying hexokinase II (HK2).
HK2↓, HK2 dissociation from mitochondria, release of apoptosis-inducing factor (AIF), and induction of apoptosis
AIF↓,
Apoptosis↑,
NK cell↑, In the latter, tumor regression was accompanied by increased circulating CD4+, CD8+, and NK cells, enhanced tumor-associated macrophage infiltration, and reduced local immunosuppression
eff↑, Upon oral administration of 3-BP-based agent KAT-101, the 3-BP derivative, being structurally similar to lactic acid, specifically binds to and enters cancer cells through monocarboxylic acid transporters (MCTs)
Glycolysis↓, KAT-101 interferes with both glycolysis and mitochondrial oxidative phosphorylation (OxPhos), thereby depleting adenosine triphosphate (ATP) levels and thus limits energy supply needed by cancer cells to proliferate.
OXPHOS↓,
ATP↓,
TumCP↓,
Apoptosis↑, This induces cancer cell apoptosis and prevents cancer cell proliferation.
HK2↓, In addition, KAT-101 is able to release mitochondrial-bound hexokinase (HK) II (HK2)
MPT↑, increases the formation of mitochondrial permeability transition pores (MPTPs), which induces apoptosis.
LDH↓, KAT-101 also inhibits a variety of enzymes, including lactate dehydrogenase (LDH), pyruvate dehydrogenase (PDH) and pyruvate dehydrogenase kinase (PDHK).
PDH↓,
other↝, Since the use of ALA-based drugs for tumor diagnosis or therapy depends on preferential PpIX tumor accumulation, we begin this review with an overview of PpIX biosynthesis from ALA and end with the prospect of combining the diagnostic and therapeutic
ROS↑, These components individually are not harmful but become cytotoxic when combined due to the generation of reactive oxygen species (ROS) via type I and II photochemical reactions.
other↝, ALA was known to cause endogenous PpIX accumulation in human lymphocytes in the 1970s [15].
mtDam↑, which causes direct mitochondrial structural damage and Ca2+ release [24].
Ca+2↑,
ER Stress↑, ALA-PDT is known to damage the endoplasmic reticulum (ER) and cause Ca2+ release, triggering apoptosis through ER-stress signaling [25].
Apoptosis↑,
TumAuto↑, Lastly, ALA-PDT is also known to induce autophagy, the degradation of cellular components by lysosomes.
other↝, ALA administration exhibits red fluorescence and photosensitizing activity upon light activation.
Dose↝, Although blue and red light-emitting diode (LED) illuminators are commonly used as the light source to activate ALA and MAL for PDT of AK lesions, natural daylight is emerging as an attractive and convenient alternative.
Imm↑, ALA-PDT not only directly kills tumor cells but also elicits potent immune responses with important implications in the long-term therapeutic outcome.
OXPHOS↑, A549 exposed to ALA exhibited enhanced oxidative phosphorylation, which was indicated by an increase in COX protein expression and oxygen consumption.
OCR↑,
Warburg↓, These data demonstrate that ALA inhibits the Warburg effect and induces cancer cell death.
ROS↑, ALA significantly increased O2-generation
over 4 h
SOD2↑, ALA stimulates MnSOD, catalase and HO-1 protein expression.
Catalase↑,
HO-1↑,
Casp3↑, ALA induced an increase in the protein expression
of activated (cleaved) caspase-3.
Apoptosis↑, these data demonstrate that ALA induced caspase-
dependent apoptosis in A549 cells.
AntiCan↑, All treatments resulted in anticancer effects depicted by cell cycle arrest and apoptosis, with TQ demonstrating greater efficacy than CQ10, both with and without 5-FU.
TumCCA↑,
Apoptosis↑,
eff↑,
Bcl-2↓, However, 5-FU/TQ/CQ10 triple therapy exhibited the most potent pro-apoptotic activity in all cell lines, portrayed by the lowest levels of oncogenes (CCND1, CCND3, BCL2, and survivin)
survivin↓,
P21↑, and the highest upregulation of tumour suppressors (p21, p27, BAX, Cytochrome-C, and Cas-
pase-3).
p27/CDKN1B↑,
BAX↑,
Cyt‑c↑,
Casp3↑,
PI3K↓, The triple therapy also showed the strongest suppression of the PI3K/AKT/mTOR/HIF1α pathway, with a concurrent increase in its endogenous inhibitors (PTEN and AMPKα) in all cell lines used.
Akt↓,
mTOR↓,
Hif1a↓,
PTEN↑,
AMPKα↑,
PDH↑, triple therapy favoured glucose oxidation by upregulating PDH, while decreasing LDHA and PDHK1 enzymes.
LDHA↓,
antiOx↓, most significant decline in antioxidant levels and the highest increases in oxidative stress markers
ROS↑,
AntiCan↑, This study is the first to demonstrate the superior anticancer effects of TQ compared to CQ10, with and without 5-FU, in CRC treatment.
ROS↑, AF primarily functions as a pro-oxidant by inhibiting thioredoxin reductase (TrxR), an antioxidant enzyme overexpressed in ovarian cancer.
TrxR↓, The primary mechanism of action of auranofin is to act as a pro-oxidative agent, increasing the production of reactive oxygen species (ROS) as a consequence of inhibiting the thioredoxin reductase (TrxR) anti-oxidant system
MMP↓, triggers the depolarization of the mitochondrial membrane, and kills HGSOC cells by inducing apoptosis.
Apoptosis↑,
eff↓, Notably, AF-induced cell death was abrogated by the ROS-scavenger N-acetyl cysteine (NAC).
Casp3↑, lethality of AF was associated with the activation of caspases-3/7 and the generation of DNA damage
Casp7↑,
DNAdam↑,
eff↑, Finally, when AF and L-BSO were combined, we observed synergistic lethality against HGSOC cells, which was mediated by a further increase in ROS and a decrease in the levels of the antioxidant GSH.
GSH↓,
angioG↓, Additionally, auranofin has been shown to inhibit angiogenesis
ChemoSen↑, In this study, we identified the mechanisms of cytotoxicity induced by auranofin in HGSOC cells that have different clinical sensitivities to platinum.
cl‑PARP↑, the cleavage of poly-ADP ribose polymerase (PARP), and the polyubiquitination of proteins
eff↑, synergistic lethal interaction between auranofin and a second pro-oxidant agent, the glutathione (GSH) inhibitor, L-buthionine sulfoximine (L-BSO);
IL6↓, This gold(I) compound has anti-inflammatory properties because it reduces IL-6 expression via inhibition of the NF-κB-IL-6-STAT3 signaling pathway.
NF-kB↓,
ATF2↓,
TrxR↓, by inhibiting redox enzymes such as thioredoxin reductase, auranofin increases cellular oxidative stress and promotes apoptosis.
ROS↑,
Apoptosis↑,
IL6↓, Recently, it was reported that auranofin reduced by 95% SARS-CoV-2 RNA in infected human cells in vitro and decreased SARS-CoV-2-induced cytokine expression, including IL-6.
Dose↑, After 14 days of treatment with 21 mg/day auranofin, plasma gold concentration reached 1.18 µM to 2.21 µM ‘auranofin equivalent’
AntiTum↑, Over the last twenty years, AF has also been repurposed as an antitumor, antiviral, and antibacterial drug.
Bacteria↓,
TrxR↓, ability to inhibit thioredoxin reductase (TrxR) and disrupt redox homeostasis, leading to selective cytotoxicity in cancer cells.
ChemoSen↑, synergistic effects observed when AF is combined with chemotherapeutics, targeted therapies, or immune modulators.
Dose↝, Patients received AF orally twice daily on days 1–28. atients received AF orally, 6 mg in the morning and 6 mg in the evening.
ROS↑, AF induces oxidative stress and apoptosis in cancer cells by disrupting redox homeostasis, while sirolimus inhibits mTOR signaling.
Apoptosis↑,
mTOR↓,
RadioS↑, AF at 3–10 μM is a potent radiosensitizer in vitro
ROS↑, . The first one is linked to an oxidative stress, as scavenging of reactive oxygen species (ROS)
eff↓, N-acetyl cysteine counteracted radiosensitization. (NAC)
mt-OCR↓, We also observed a decrease in mitochondrial oxygen consumption with spared oxygen acting as a radiosensitizer under hypoxic conditions.
DNAdam↑, Overall, radiosensitization was accompanied by ROS overproduction, mitochondrial dysfunction, DNA damage and apoptosis
Apoptosis↑,
TrxR↓, targeting thioredoxin reductase (TrxR)
eff↑, a simultaneous disruption of the thioredoxin and glutathione systems by the combination of AF and buthionine sulfoximine was shown to significantly improve tumor radioresponse.
TrxR↓, Auranofin (Au), an inhibitor of thioredoxin reductase, is a known anti‑cancer drug
AntiCan↑,
TumCG↓, Au inhibited the growth of HeLa cells with an IC50 of ~2 µM at 24 h.
Apoptosis↑, This agent induced apoptosis and necrosis, accompanied by the cleavage of poly (ADP‑ribose) polymerase and loss of mitochondrial membrane potential.
necrosis↑,
cl‑PARP↑,
MMP↓,
ROS↑, With respect to the levels of ROS and GSH, Au increased intracellular O2•- in the HeLa cells and induced GSH depletion.
GSH↓,
eff↓, The antioxidant, N‑acetyl cysteine, not only attenuated apoptosis and necrosis in the Au‑treated HeLa cells, but also decreased the levels of O2•- and GSH depletion in the cells.
TrxR↓, Auranofin mainly targets the anti-oxidative system catalyzed by thioredoxin reductase (TrxR), which protects the cell from oxidative stress and death in the cytoplasm and the mitochondria.
ROS↑, Inhibiting TrxR dysregulates the intracellular redox state causing increased intracellular reactive oxygen species levels, and stimulates cellular demise
eff↑, TrxR is over-expressed in many cancers as an adaptive mechanism for cancer cell proliferation, rendering it an attractive target for cancer therapy, and auranofin as a potential therapeutic agent for cancer.
Apoptosis↑, promotion of ASK-induced apoptosis, and blockage of cell growth, proliferation, and survival due to reduced AKT activity and NF-kB- and p53-mediated transcription.
TumCG↓,
TumCP↓,
Akt↓,
NF-kB↓,
DNAdam↑, DNA damage
eff↝, auranofin inhibits TrxR1 in a p53-independent manner
eff↓, Pre-treatment with NAC counteracted the cancer cell killing effects of auranofin,
PI3K↓, auranofin induces cytotoxicity in human pancreatic adenocarcinoma and non-small cell lung cancer via the inhibition of the PI3K/AKT/mTOR pathway
Akt↓,
mTOR↓,
Hif1a↓, auranofin inhibits the cancer cell response to hypoxia, demonstrated by a decrease in HIF-1 𝛼 expression and VEGF secretion upon auranofin treatment under hypoxic conditions
VEGF↓,
Casp3↑, auranofin was shown to induce caspase-3-mediated apoptosis in human ovarian carcinoma SKOV-3 cells
CSCs↓,
ATP↓, it was found that auranofin inhibits ABCG2 function by depleting cellular ATP via inhibition of glycolysis [96]
Glycolysis↓,
eff↑, auranofin synergizes with another Trx1 inhibitor, piperlongumine, in killing gastric cancer cells in association with ROS-mediated ER stress response and mitochondrial dysfunction.
eff↑, when the gold complex is combined with either selenite or tellurite [104]
MMP↓, Increased ROS induced by AUR causes decreased membrane potential in the mitochondrial membrane, resulting in a decrease in anti-apoptotic proteins, caspase-dependent cell death, and translocation of apoptosis-inducing factor (AIF)
AIF↑,
toxicity↓, Auranofin is considered safe for human use in treating rheumatoid arthritis; thus, this gold derivative can reach the clinic for other diseases relatively quickly and at a low cost
TumCP↓,
Apoptosis↑,
NF-kB↓,
p50↓,
cycD1/CCND1↓,
Bcl-xL↓,
ChemoSen↑, AS-IV can enhance paclitaxel-induced cell apoptosis and cell cycle arrest at G2/M phase
angioG↓,
ChemoSen↑, Enhances Sensitivity to Cisplatin
TumCI↓,
Apoptosis↑,
Symptoms↓,
PIK3CA↓,
Akt↓,
Bcl-2↓,
AntiTum↑,
Apoptosis↑,
Bcl-2↓,
BAX↑,
Casp3↑,
Casp9↑,
Bax:Bcl2↑, ratio of Bax to Bcl-2 was significantly enhanced by the APS to cisplatin
TumCG↓,
TumCCA↑, cell cycle arrest (G2 phase)
Apoptosis↑,
*IL2↑, in peripheral blood
*TNF-α↑, in peripheral blood
*IFN-γ↑, in peripheral blood
AntiTum↑, APS has been increasingly used in cancer therapy owing to its anti-tumor ability as it prevents the progression of prostate, liver, cervical, ovarian, and non-small-cell lung cancer by suppressing tumor cell growth and invasion and enhancing apoptosi
TumCG↓,
TumCI↓,
Apoptosis↑, after APS treatment, the apoptosis of HepG2 cells is accelerated (57).
Imm↑, APS enhances the sensitivity of tumors to antineoplastic agents and improves the body’s immunity
Bcl-2↓, Huang et al. proposed that APS induces H22 (a hepatocellular cancer [HCC] cell line) apoptosis by downregulating Bcl-2 and upregulating Bax expression (56).
BAX↑,
Wnt↓, downregulating the Wnt/β-catenin signaling pathway.
β-catenin/ZEB1↓,
TumCG↓, APS effectively inhibited the growth of MDA-MB-231 (a human breast cancer [BC] cell line) graft tumor (58)
miR-133a-3p↑, apoptosis rate of human osteosarcoma MG63 cells increased owing to the upregulation of miR-133a and inactivation of the JNK signaling pathways (71).
JNK↓,
Fas↑, Li and Shen found that APS can induce apoptosis by activating the Fas death receptor pathway.
P53↑, Zhang et al. showed that APS could activate p53 and p21 and inhibit the expression of Notch1 and Notch3 in vitro, ultimately inhibiting cell proliferation and promoting their apoptosis
P21↑,
NOTCH1↓,
NOTCH3↓,
TumCP↓,
TumCCA↑, Liu et al. found that APS induced the cell cycle of bladder cancer UM-UC-3 to stop in the G0/G1 phase, thus inhibiting its proliferation
GPx4↓, APS was found to reduce GPX4 expression, inhibit the activity of the light chain subunit SLC7A11 (xCT), and promote the formation of BECN1-xCT complex by activating AMPK/BECN1 signaling.
xCT/SLC7A11↓,
AMPK↑,
Beclin-1/ATG6↑,
NF-kB↓, APS could control the proliferation of lung cancer cells (A549 and NCI-H358 cells) by inhibiting the NF-κB signaling pathway (97)
EMT↓, APS treatment led to reduced EMT markers (vimentin, AXL) and MIF levels in cells.
Vim↓,
TumMeta↓, APS inhibits Lewis lung cancer growth and metastasis in mice by significantly reducing VEGF and EGFR expression in cancerous tissues
VEGF↓,
EGFR↓,
eff↑, Nano-drug delivery systems can increase efficiency and reduce toxicity
eff↑, Jiao et al. developed selenium nanoparticles modified with macromolecular weight APS and observed positive results in hepatoma treatment
MMP↓, Subsequent investigations revealed that APS can decrease the ΔΨm values and Bcl-2, p-PI3K, P-gp, and p-AKT levels while elevating Bax expression.
P-gp/ABCB1↓,
MMP9↓, downregulation of MMP-9 expression,
ChemoSen↑, Li et al. observed that APS could enhance the sensitivity of SKOV3 ovarian cancer cells to CDDP treatment by activating the mitochondrial apoptosis pathway and JNK1/2 signaling pathway
SIRT1↓, APS significantly suppressed SIRT1 and SREBP1 expression, decreased cholesterol and triglyceride levels in PC3 and DU145, and attenuated cell proliferation.
SREBP1/SREBF1↓,
TumAuto↑, APS can induce autophagy in colorectal cancer cells by inhibiting the PI3K/AKT/mTOR axis and the development of cancer cells.
PI3K↓,
mTOR↓,
Casp3↑, Shen found that APS elevated caspase-9, caspase-3, and Bax protein levels, decreased Bcl-2 protein expression, and inhibited CD133 and CD44 co-positive colon cancer stem cell proliferation time
Casp9↑,
CD133↓,
CD44↓,
CSCs↓,
QoL↑, QOL was significantly improved as indicated by the reduction in pain and improvement in appetite
AntiCan↑, Preclinical studies indicate that APS exerts significant anti-liver cancer effects through multiple biological actions, including the promotion of apoptosis, inhibition of proliferation, suppression of epithelial–mesenchymal transition, regulation of
Apoptosis↑,
TumCP↓,
EMT↓,
Imm↑, improving host immune response
ChemoSen↑, APS exhibits synergistic effects when combined with conventional chemotherapeutics and interventional treatments such as transarterial chemoembolisation, improving efficacy and reducing toxicity.
BioAv↓, limitations such as low bioavailability and a lack of large-scale clinical trials remain challenges for clinical translation.
TumCG↓, APS significantly inhibited tumour growth in H22-bearing mice with a dose-dependent effect (100, 200, 400 mg/kg), with the 400 mg/kg group achieving a tumour inhibition rate of 59.01%
IL2↑, APS enhance the thymus and spleen indices and elevates the key cytokines, including IL-2, IL-12, and TNF-α.
IL12↑,
TNF-α↑,
P-gp/ABCB1↓, APS reversed chemoresistance by downregulating P-glycoprotein and MDR1 mRNA expression
MDR1↓,
QoL↑, These effects contributed to improved treatment tolerance and enhanced quality of life [39].
Casp↑, APS can activate both the intrinsic and extrinsic apoptotic pathways, leading to caspase activation and DNA fragmentation
DNAdam↑,
Bcl-2↓, Mechanistically, APS downregulate antiapoptotic proteins such as Bcl-2 while upregulating proapoptotic proteins such as Bax and cleaved caspase-3.
BAX↑,
MMP↓, APS have been shown to disrupt the mitochondrial membrane potential and promote the release of cytochrome c, thereby enhancing apoptotic cascades in hepatocellular carcinoma models.
Cyt‑c↑,
NOTCH1↓, APS (0.1, 0.5, and 1.0 mg/mL) were shown to reduce both mRNA and protein levels of Notch1 in a concentration-dependent manner.
GSK‐3β↓, APS significantly inhibited the proliferation of HepG2 cells by downregulating the expression of glycogen synthase kinase-3β (GSK-3β), with 200 μg/mL being the most effective concentration.
TumCCA↑, APS exerted these effects by inducing cell cycle arrest at the G2/M and S phases, thereby impeding tumour cell proliferation [35].
GSH↓, HepG2 cells. APS also reduced intracellular glutathione (GSH) levels, increased reactive oxygen species (ROS) and lipid peroxidation levels, and elevated intracellular iron ion concentrations—all in a dose-dependent manner.
ROS↑,
lipid-P↑,
c-Iron↑,
GPx4↓, APS treatment led to the downregulation of GPX4 and upregulation of ACSL4, indicating that APS promotes ferroptosis in liver cancer cells.
ACSL4↑,
Ferroptosis↑,
Wnt↓, inhibit the expression of key proteins involved in the Wnt/β-catenin signalling pathway
β-catenin/ZEB1↓,
cycD1/CCND1↓, by downregulating the key oncogenic targets, including β-catenin, C-myc, and cyclin D1, which subsequently reduces Bcl-2 expression and activates the apoptotic cascade in HepG2 liver cancer cells.
Akt↓, It also inhibited the Akt/p-Akt signalling pathway.
PI3K↓, APS inhibit the PI3K/AKT/mTOR signalling pathway, which is a central negative regulator of autophagy.
mTOR↓,
CXCR4↓, PS upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker vimentin and the chemokine receptor CXCR4 at both mRNA and protein levels, suggesting that APS suppress liver cancer cell growth and metastasis by inhibiting
Vim↓,
PD-L1↓, APS interfere with immune checkpoint signalling by downregulating Programmed death-ligand 1 (PD-L1) expression on tumour cells.
eff↑, The preparation of polysaccharide–SeNP composites typically involves using sodium selenite (Na2SeO3) as the precursor and ascorbic acid (Vc) as the reducing agent, with synthesis carried out via a chemical reduction method in a polysaccharide solutio
eff↑, Mechanistic investigations revealed that AASP–SeNPs elevated intracellular ROS levels and reduced the mitochondrial membrane potential (∆Ψm).
ChemoSen↑, APS enhance doxorubicin-induced endoplasmic reticulum (ER) stress by reducing O-GlcNAcylation levels, thereby promoting apoptosis of liver cancer cells.
ChemoSen↑, APS inhibited BEL-7404 human liver cancer cell growth in a concentration-dependent manner and showed stronger cytotoxicity when combined with cisplatin.
chemoP↑, APS protects against chemotherapy-induced liver injury, particularly that caused by CTX, through antiapoptotic mechanisms
*ROS↑, AgNP exposure significantly and dose-dependently decreased the cell viability, induced reactive oxygen species (ROS) generation and led to early apoptosis in HUVECs.
*Apoptosis↑,
*NRF2↝, AgNPs could disrupt the inactivation of the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant response, which is considered another important element for oxidative stress caused by AgNPs in HUVECs.
| - |
in-vitro, |
GBM, |
U251 |
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- |
in-vitro, |
GBM, |
U87MG |
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- |
in-vitro, |
GBM, |
GL26 |
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- |
in-vitro, |
Cerv, |
HeLa |
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- |
in-vitro, |
CRC, |
RKO |
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AntiCan↑, Among the various NPs, silver nanoparticles (AgNPs) have garnered attention due to their cytotoxic and genotoxic properties in cancer cells.
eff↑, Our results demonstrate that UiO-66-NH2@AgNPs@Cis-Pt and its combinations exhibit enhanced cytotoxicity compared to individual components such as AgNPs and Cis-Pt.
EPR↑, Their nanometric structure allows them to easily penetrate and accumulate in tumour tissues either actively, via targeting systems [6,7,8], or passively, by taking advantage of tumour angiogenesis and the enhanced permeation and retention (EPR) effe
selectivity↑,
ROS↑, Once inside, AgNPs induce an increase in the production of reactive oxygen species (ROS) and cause mitochondrial dysfunctions, caspases activation, apoptosis, autophagy, and DNA damage
Casp↑,
Apoptosis↑,
DNAdam↑,
tumCV↓, figure 8
eff↑, One of the primary characteristics of AgNPs is their ability to release Ag+ ions from their surface in response to low pH or oxidation.
Apoptosis↑, The involvement of mitochondrial pathway of cell death in the Ag-CS NCs induced apoptosis was evident from the depolarization of mitochondrial membrane potential (ΔΨ(m)).
MMP↓,
Casp3↑, up-regulation of caspase 3 expression
ROS↑, increased production of intracellular ROS due to Ag-CS NCs treatment indicated that the oxidative stress could augment the induction of apoptosis in HT 29 cells
eff↑, use of significantly low concentration of Ag NPs impregnated in chitosan nanocarrier is a much superior approach in comparison to the use of free Ag NPs in cancer therapy.
OS↑, Results indicate that the AgNPs were efficient in prolongation of life span, reduction of tumor volume and body weight in tumor animals.
TumVol↓,
Weight↑,
AntiTum↑, AgNPs are potent in antitumor activity and the molecular mechanism is by the induction of apoptosis through the mitochondrial dependent and independent pathways.
Apoptosis↑,
mtDam↑,
Apoptosis↑, AgNPs induced apoptosis in HepG2 cells through the particle-specific effects on mitochondria.
tumCV↓, the numbers of A2780 (bulk cells) and ALDH+/CD133+ colonies were significantly reduced
CSCs↓,
selectivity↑, induced apoptosis in pancreatic CSCs and cancer cell lines, but had no effect on human normal pancreatic epithelial cells
Apoptosis↑,
ROS↑, figure 5, AgNPs induces apoptosis by oxidative stress
LDH↓, figure 5 (leakage outside the cell increases)
Casp3↑, AgNPs treated cells shows up-regulation of caspase-3, bax, bak, and c-myc, genes
BAX↑,
Bak↑,
cMyc↑,
MMP↓, and loss of mitochondrial membrane potential.
tumCV↑, AgNPs exhibit significant cytotoxic and apoptotic effects in lung cancer cell lines through mechanisms involving gene regulation, reactive oxygen species (ROS) production, and mitochondrial depolarization.
ROS↑,
MMP↓,
TumCCA↑, dose-dependent reductions in cell viability, cell cycle arrest, and apoptosis induction.
Apoptosis↑,
angioG↓, inhibit angiogenesis
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in-vitro, |
BC, |
MDA-MB-231 |
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|
ROS↑, Caf-AgNPs significantly increased ROS, malondialdehyde, COX-2, IL-1β, and TNF-α level in BC cells, which was accompanied by a decrease in glutathione levels.
MDA↑,
COX2/PTGS2↑,
IL1β↑,
TNF-α↑,
GSH↓,
Cyt‑c↑, increased levels of cytosolic cytochrome c, caspase-3, and Bax proteins, as well as a significant decrease in Bcl-2 expression and Bcl-2/Bax ratio
Casp3↑,
BAX↑,
Bcl-2↓,
LDH↓, Cancer cells subjected to Caf-AgNPs demonstrated elevated lactate dehydrogenase (LDH) membrane leakage
cycD1/CCND1↓, notable downregulation of cyclin D1 and cyclin-dependent kinase 2 (CDK2) mRNA expression
CDK2↓,
TumCCA↑, several mechanisms for cellular destruction, including cell cycle arrest, oxidative stress induction, modulation of the inflammatory response, and mitochondrial apoptosis
mt-Apoptosis↑,
TumCMig↓, Our results showed that C-AgNPs significantly inhibited MCF-7 cell migration
Apoptosis↑, gene expression analysis indicated the induction of apoptosis by upregulation of pro-apoptotic genes BAX and P53 and downregulation of Bcl-2.
BAX↑,
P53↑,
Bcl-2↓,
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in-vitro, |
Lung, |
A549 |
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in-vitro, |
PC, |
MIA PaCa-2 |
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Nor, |
HEK293 |
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AntiCan↑, (AgNPs) have emerged as promising multifunctional agents in biomedical applications due to their notable antimicrobial and anticancer properties.
selectivity↑, demonstrated significant cytotoxic effects on cancer cells while sparing normal cells
Apoptosis↑, Apoptosis induction, cell cycle arrest, and gene expression analyses further validated their anticancer efficacy.
TumCCA↑,
Bacteria↓, Figure 6a,b show the inhibition zones of 10 µg ampicillin and 10, 50, 100, and 150 μg/mL AgNPs against bacteria on agar for two repeated tests.
tumCV↓, AgNPs at concentrations of 6.3, 6.8, 7.5, 8.3, 9.4, 10.7 and 12.5 µg/mL for 24 h. After treatment, a significant decrease in cell viability was observed in different cancer cell types,
selectivity↑, The toxic effect was weaker in healthy cells than in cancer cells
Apoptosis↑, Fig. 8a–c, a significant increase (p < 0.01; p < 0.001) in the rate of early and late apoptotic cells was observed in A549, MIA PaCa-2 and PC-3 cells.
TumCCA↑, accompanied by arrest in the S phase and, particularly, the G2/M phase.
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in-vitro, |
BC, |
MCF7 |
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in-vitro, |
BC, |
T47D |
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in-vitro, |
BC, |
MDA-MB-231 |
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TumCD↑, AgNPs showed potent cytotoxicity in breast cancer cells, no matter whether they were tamoxifen sensitive or resistant.
other↓, Next, we found that a long noncoding RNA, XLOC_006390, was decreased in AgNPs-treated breast cancer cells, coupled to inhibited cell proliferation, altered cell cycle and apoptotic phenotype.
P53↑, According to the literature, AgNPs may induce cancer cells apoptosis by activating p53, so as to achieve the antitumor effect
TumCCA↑, We found that AgNPs treatment at 150 μg/ml could induce G0/G1 cell cycle arrest
Apoptosis↑, and promote both early apoptosis and late apoptosis/necrosis rate
ChemoSen↑, AgNPs-based approaches provided a potential way to fight drug resistance and reduce the toxicity related to chemotherapy drugs
tumCV↓, One of the highlights of this study is that AgNPs have strong cytotoxicities on all the breast cancer cell lines and clinically isolated breast cancer cells, with the IC50s at about 150 μg/ml for all
γH2AX↑, early apoptosis markers (γH2AX), was also significantly upregulated by AgNPs treatment
SOX4↓, AgNPs can inhibit the SOX4 expression by regulating XLOC_006390/miR-338-3p axis.
Apoptosis↑, According to our findings AgNPs are able to kill osteosarcoma cells independently from their actual p53 status and induce p53-independent cancer cell apoptosis.
other↑, AgNPs kill cells through a Trojan-horse type mechanism, suggesting that the intracellularly accumulated nanoparticles release toxic silver ions
ROS↑, Those ions induce the generation of reactive oxygen species (ROS)
eff↑, t has been reported that 5 nm AgNPs were more toxic compared to 20 nm and 50 nm particles in four different cell lines
P53↝, Nearly 50% of all human cancers have been characterised by impaired p53 function which attenuates therapeutic efficacy. The level of p53 protein increased markedly upon 20 μM of 5 nm and 85 μM of 35 nm sized AgNP treatments
Apoptosis↑, Induction of apoptosis was verified by immunostaining U2Os and Saos-2 cells with cleaved caspase 3 specific antibody after treatments with 20 μM of 5 nm and with 85 μM of 35 nm sized AgNPs for 24 h
cl‑Casp3↑,
survivin↓, as decreased survivin and elevated caspase 3 mRNA levels were measured
MMP↓, Decreased mitochondrial membrane potential was detected in 5 nm and 35 nm AgNPs treated U2Os (a) and Saos-2
Cyt‑c↑, Elevated levels of cytoplasmic cytochrome c was detected in 5 nm and 35 nm AgNP-treated U2Os and Saos-2 cells
toxicity↝, The effect of Ag ions was also investigated and compared with that of AgNPs, as it is anticipated that Ag ions will be released from AgNPs, which may be responsible for their toxicity.
tumCV↓, Cell viability tests indicated high sensitivity of Jurkat T cells when exposed to AgNPs compared to Ag ions
ROS↑, AgNPs and Ag ions induce similar levels of cellular reactive oxygen species during the initial exposure period and; after 24 h, they were increased on exposure to AgNPs compared to Ag ions, which suggest that oxidative stress may be an indirect caus
p38↑, AgNPs exposure activates p38 mitogen-activated protein kinase through nuclear factor-E2-related factor-2 and nuclear factor-kappaB signaling pathways, subsequently inducing DNA damage, cell cycle arrest and apoptosis.
NRF2↓,
NF-kB↝,
DNAdam↑,
Apoptosis↑,
ROS↑, This review focus on the abilities of nanoparticles to induce oxidative stress, prevent proliferation, and trigger apoptosis in cancer cells.
TumCP↓,
Apoptosis↑,
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Pca, |
LNCaP |
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in-vitro, |
Pca, |
DU145 |
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selectivity↑, Both AgNPs and G-AgNPs were cytotoxic only to CRPC cells and not to hormone-sensitive ones and their effect was higher after functionalization showing the potential of glucose to favor AgNPs’ uptake by cancer cells.
ROS↑, NPs increased the ROS, inducing mitochondrial damage, and arresting cell cycle in S Phase, therefore blocking proliferation, and inducing apoptosis.
mtDam↑,
TumCCA↑,
TumCP↓,
Apoptosis↑,
MMP↓, AgNPs were able to depolarize the cells’ mitochondria to 32.74% and 10.36%, respectively
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in-vitro, |
Kidney, |
786-O |
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ROS↑, AgNPs are cytotoxic to 786-O cells, a ccRCC cell line, entering through endocytosis, increasing ROS, depolarizing mitochondrial membrane, and blocking the cell cycle, leading to a reduction of proliferation capacity and apoptosis.
MMP↑,
TumCCA↑,
TumCP↓,
Apoptosis↑,
RadioS↑, 786-O is intrinsically resistant to radiation, but after AgNPs’ administration, radiation induces cytotoxicity through mitochondrial membrane depolarization and S phase blockage.
EPR↑, cellular uptake of the AgNPs results indicated that the AgNPs accumulated within the cell.
BAX↑, Bax, Bcl-2, caspase-3 (CASP3), caspase-9 (CASP9)
Bcl-2↑,
Casp3↑,
Casp9↑,
DNAdam↑, apoptotic effects of the AgNPs through DNA fragmentation test, flow cytometry and cell cycle analysis indicated the induction of apoptosis in the A549 cell line.
TumCCA↑,
Apoptosis↑,
ROS↑, significant increase in ROS and lipid peroxidation (LPO), along with a decrease in MMP and glutathione (GSH) levels.
lipid-P↑,
MMP↓,
GSH↓,
TumCCA↑, significant increase in ROS and lipid peroxidation (LPO), along with a decrease in MMP and glutathione (GSH) levels.
Apoptosis↑,
Necroptosis↑,
TumCD↑, AgNPs-induced cell death in HeLA cells suggested the anticancer potential of ND-AgNPs.
Dose↝, ND-AgNPs at 10, 25, and 50 µg/ml concentration
eff↑, electronic microscopy experiments revealed that AgNP20 can rapidly interact with the cell membrane, penetrate neutrophils, localize in vacuole-like structures, and be randomly distributed in the cytosol after 24 h.
Apoptosis↑, AgNP20 induced apoptosis
eff↑, AgNPs were demonstrated to be able to enter K562 cells (a CML cell line) in a dose-dependent manner and locate in endosomes
ROS↑, Reactive oxygen species (ROS) could be generated upon AgNPs exposure and cause cytotoxicity and apoptosis.
Apoptosis↑,
eff↓, alterations caused by AgNPs exposure could be reversed by the addition of Vitamin C (an antioxidant).
ROS↑, The gAgNPs induced more ROS in the HuH-7 cells than in the CHANG cells.
selectivity↑, HuH-7 cells showed an increased sensitivity to gAgNPs than the CHANG cells.
DNAdam↑, higher concentrations of gAgNPs may induce significant cytotoxicity and cause DNA damage and apoptosis.
Apoptosis↑,
GSH↓, The level of glutathione was decreased (Figure 4B) and lipid peroxide was increased in HuH-7 cells than CHANG cells (Figure 4A).
lipid-P↑,
MMP↓, indicating loss of MMP
DNAdam↑, higher DNA damage was seen in HuH-7 cells than CHANG cells
tumCV↓, decreased cell viability in a concentration-dependent manner and the IC50 of 75 μg/mL for Ag NPs
ROS↑, Ag NPs cytotoxicity was associated with induction of ROS and cell apoptosis in HepG2 cell line
Apoptosis↑,
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in-vitro, |
Lung, |
A549 |
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in-vivo, |
Lung, |
A549 |
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Apoptosis↑, Silver nanoparticles (AgNPs) have shown great potential as therapeutic agents due to their ability to cause apoptotic cell death in cancer cells.
VEGF↓, suppressing the VEGF signaling pathway, repressing p53-mediated pathways, promoting cell cycle arrest,
P53↓,
TumCCA↑,
ROS↑, we found that AgNPs induced ROS generation
AntiTum↑, AgNPs exhibit similar antitumoral effects on both A549 and A549/DDP-bearing mice.
eff↑, AgNPs are internalized by cells far more effectively than free Ag+ under identical exposure conditions
ATP↓, AgNPs exposure also decreased basal respiration (52.3 ± 4.6 pmol/min/106 cells), maximal respiration (109.2 ± 12.2 pmol/min/106 cells), ATP production (
eff↑, These results explain why AgNPs remain effective against cisplatin-resistant A549 cells.
CTR1↑, recent studies have shown that AgNPs treatment significantly upregulates CTR1
Showing Research Papers: 1 to 50 of 1601
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1601
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 1, Catalase↑, 1, Ferroptosis↓, 1, Ferroptosis↑, 1, GPx4↓, 2, GSH↓, 8, HO-1↑, 1, c-Iron↑, 1, lipid-P↑, 3, MDA↑, 2, MFN2↑, 1, NRF2↓, 1, OXPHOS↓, 1, OXPHOS↑, 1, ROS↑, 29, mt-ROS↑, 1, SOD2↑, 1, TrxR↓, 6, xCT/SLC7A11↓, 1, xCT/SLC7A11↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↓, 1, AIF↑, 2, ATP↓, 4, MMP↓, 12, MMP↑, 1, MPT↑, 1, mtDam↑, 3, OCR↑, 1, mt-OCR↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACSL4↑, 1, AMPK↑, 2, cMyc↑, 1, Glycolysis↓, 5, HK2↓, 6, LDH↓, 3, LDHA↓, 1, NADPH↓, 1, PDH↓, 1, PDH↑, 1, PIK3CA↓, 1, PPP↓, 1, SIRT1↓, 1, SREBP1/SREBF1↓, 1, Warburg↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 7, p‑Akt↓, 1, Apoptosis↑, 50, mt-Apoptosis↑, 1, ATF2↓, 1, Bak↑, 1, BAX↑, 9, Bax:Bcl2↑, 2, Bcl-2↓, 7, Bcl-2↑, 1, Bcl-xL↓, 1, Casp↑, 2, Casp3↑, 10, cl‑Casp3↑, 2, cl‑Casp3⇅, 1, Casp7↑, 1, Casp9↑, 4, Cyt‑c↑, 5, Fas↑, 1, Ferroptosis↓, 1, Ferroptosis↑, 1, JNK↓, 1, MAPK↝, 1, Necroptosis↑, 1, necrosis↑, 1, p27/CDKN1B↑, 1, p38↑, 3, survivin↓, 4, TumCD↑, 4,
Kinase & Signal Transduction(tgid=6) ⓘ
AMPKα↑, 2,
Transcription & Epigenetics(tgid=7) ⓘ
other↓, 1, other↑, 1, other↝, 4, tumCV↓, 7, tumCV↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1/ATG6↑, 1, p‑Beclin-1/ATG6↑, 1, TumAuto↑, 4,
DNA Damage & Repair(tgid=10) ⓘ
BRCA2↓, 1, DNAdam↑, 9, P53↓, 1, P53↑, 4, P53↝, 1, cl‑PARP↑, 4, γH2AX↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK2↓, 1, cycD1/CCND1↓, 3, P21↑, 2, TumCCA↑, 17,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD133↓, 1, CD44↓, 1, CSCs↓, 3, EMT↓, 2, FOXO3↑, 1, GSK‐3β↓, 1, p‑GSK‐3β↓, 1, mTOR↓, 5, mTOR↝, 1, NOTCH1↓, 2, NOTCH3↓, 1, PI3K↓, 4, PTEN↑, 1, TumCG↓, 8, Wnt↓, 2,
Migration(tgid=13) ⓘ
Ca+2↑, 1, E-cadherin↑, 1, miR-133a-3p↑, 1, MMP9↓, 1, N-cadherin↑, 1, SOX4↓, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 10, TumMeta↓, 1, Twist↓, 1, Vim↓, 2, β-catenin/ZEB1↓, 4,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, EGFR↓, 1, EPR↑, 2, Hif1a↓, 2, VEGF↓, 3,
Barriers & Transport(tgid=15) ⓘ
CTR1↑, 1, P-gp/ABCB1↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, COX2/PTGS2↑, 1, CXCR4↓, 1, IL12↑, 1, IL1β↑, 1, IL2↑, 1, IL6↓, 2, Imm↑, 3, NF-kB↓, 4, NF-kB↝, 1, NK cell↑, 2, p50↓, 1, PD-L1↓, 1, TNF-α↑, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, ChemoSen↑, 10, Dose↑, 1, Dose↝, 7, eff↓, 9, eff↑, 23, eff↝, 2, Half-Life↓, 1, MDR1↓, 1, RadioS↑, 3, selectivity↑, 9,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1, IL6↓, 2, LDH↓, 3, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 7, AntiTum↑, 6, chemoP↑, 1, OS↑, 1, QoL↑, 2, Symptoms↓, 1, toxicity↓, 2, toxicity↑, 2, toxicity↝, 1, TumVol↓, 3, TumW↓, 1, Weight↑, 1,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 2,
Total Targets: 171
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↑, 1, TRPA1↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↑, 1, GPx↑, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 1, NRF2↑, 1, NRF2↝, 1, ROS↓, 1, ROS↑, 1, SOD↑, 1, TAC↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
NADPH↑, 1, PPARγ↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IFN-γ↑, 1, IL1β↓, 1, IL2↑, 1, Inflam↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1, TNF-α↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE/β-secretase↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, eff↑, 1, Half-Life↝, 1,
Functional Outcomes(tgid=23) ⓘ
cardioP↑, 1, neuroP↑, 1, toxicity↓, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 1,
Total Targets: 38
Scientific Paper Hit Count for: Apoptosis, Apoptosis
66
Silver-NanoParticles66
Curcumin39
Magnetic Fields37
Quercetin32
Sulforaphane (mainly Broccoli)31
Berberine30
Thymoquinone28
EGCG (Epigallocatechin Gallate)27
Baicalein24
Capsaicin23
Kaempferol22
Phenethyl isothiocyanate22
Shikonin21
Ashwagandha(Withaferin A)20
Radiotherapy/Radiation20
Betulinic acid20
Garcinol20
Honokiol19
Resveratrol19
Selenite (Sodium)18
Artemisinin18
Apigenin (mainly Parsley)18
Licochalcone A17
Boron17
Gambogic Acid16
Chrysin15
Cisplatin15
Chemotherapy15
chitosan15
Dandelion Root15
Emodin15
Eugenol15
Fisetin15
Formononetin14
Nimbolide13
Graviola13
Magnolol13
Hyperoside13
Indole-3-carbinol13
Ivermectin13
Lycopene12
Metformin12
Astaxanthin12
Beta-Caryophyllene12
salinomycin12
HydroxyTyrosol12
Isobavachalcone12
Juglone12
Luteolin12
Urolithin11
Carvacrol11
Dichloroacetate10
Allicin (mainly Garlic)10
Paclitaxel/Taxol10
Chlorogenic acid10
Crocetin10
IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)10
Piperlongumine10
Selenium NanoParticles9
Photodynamic Therapy9
Copper and Cu NanoParticles9
Vitamin C (Ascorbic Acid)9
Propolis -bee glue9
chaetocin9
Cucurbitacin9
Silymarin (Milk Thistle) silibinin9
Isoliquiritigenin9
Fucoidan9
Ginkgetin9
Magnetic Field Rotating8
5-fluorouracil8
Alpha-Lipoic-Acid8
Gemcitabine (Gemzar)8
Bufalin/Huachansu8
Selenium8
Citric Acid8
Cynara scolymus/Globe Artichoke/Artichoke Extract8
Electrical Pulses8
Cynaropicrin8
Gallic acid8
Phenylbutyrate8
Rosmarinic acid7
Auranofin7
Atorvastatin7
Biochanin A7
Boswellia (frankincense)7
α-Bisabolol / Chamomile oil7
Caffeic acid7
Cinnamon7
Carvone7
Deguelin7
Lemongrass Extract/Citral7
Genistein (soy isoflavone)7
Evodiamine7
Isovitexin7
Ursolic acid6
Coenzyme Q106
Astragalus6
Fenbendazole6
Andrographis6
doxorubicin6
borneol6
Carnosic acid6
Disulfiram6
Ellagic acid6
Echinacea6
Ginkgolide B6
Hibiscus sabdariffa6
Piperine6
Terpinen-4-ol / Tea Tree Oil5
3-bromopyruvate5
Anethole/trans-Anethole5
immunotherapy5
Thymol-Thymus vulgaris5
Celecoxib5
Celastrol5
Diclofenac5
D-limonene5
Aflavin-3,3′-digallate5
Ferulic acid5
iodine5
Vitexin5
Plumbagin5
Pterostilbene5
Vitamin K24
1,8-Cineole4
Gold NanoParticles4
Ascorbyl Palmitate4
Melatonin4
Berbamine4
Brucea javanica4
Bacopa monnieri4
Bromelain4
Butyrate4
Centella asiatica / Gotu kola → asiaticoside4
Chlorophyllin4
Dichloroacetophenone(2,2-)4
isoorientin4
isoquercitrin4
itraconazole4
Lasiodin4
Licorice4
Linalool4
Parthenolide4
Spermidine3
2-DeoxyGlucose3
Aspirin3
Dipyridamole3
tamoxifen3
Baicalin3
brusatol3
Bruteridin(bergamot juice)3
Cat’s Claw3
Cannabidiol3
Date Fruit Extract3
diet FMD Fasting Mimicking Diet3
Eurycomanone3
Galloflavin3
Ginkgolic acids3
Ginkgo biloba3
Geraniol3
Ginger/6-Shogaol/Gingerol3
γ-linolenic acid (Borage Oil)3
Gossypol/AT-1013
Grapeseed extract3
Hyperthermia3
Rutin3
Inositol3
isoflavones3
Lapachol3
Lactoferrin/Talactoferrin3
Methyl salicylate / Sweet Birch oil3
Magnesium3
Niclosamide (Niclocide)3
Sanguinarine3
Psoralidin3
α-Santalol/Sandalwood oil3
VitK3,menadione3
Zerumbone2
cetuximab2
5-Aminolevulinic acid2
Ajoene (compound of Garlic)2
alpha Linolenic acid2
DTS(dibenzyl trisulphide) from Anamu2
Sorafenib (brand name Nexavar)2
Aloe anthraquinones2
beta-glucans2
Docetaxel2
Bortezomib2
Bullatacin2
Caffeic Acid Phenethyl Ester (CAPE)2
Chocolate2
irinotecan2
Polyphenols2
CUSP92
Cyclopamine2
gefitinib, erlotinib2
Ginkgo biloba-EGb 7612
Folic Acid, Vit B92
eicosapentaenoic acid2
Fennel Oil/Foeniculum vulgare2
Shilajit/Fulvic Acid2
Hydrogen Gas2
HydroxyCitric Acid2
Helleborus niger extracts – Christmas Rose2
Methylglyoxal2
Naringin2
Oleuropein2
Oleocanthal2
Orlistat2
Oxygen, Hyperbaric2
Propyl gallate2
polyethylene glycol2
Vitamin D31
Glucose1
entinostat1
Trichostatin A1
temozolomide1
Trastuzumab1
almonertinib1
epirubicin1
Lapatinib1
bempedoic acid1
Bifidobacterium1
Beta‐Lapachone1
Selenate1
Prebiotic1
Hydroxycinnamic-acid1
Vitamin E1
Carica papaya leaf extract1
Camptothecin1
Dihydrocaffeic Acid1
methylseleninic acid1
diet Methionine-Restricted Diet1
diet Short Term Fasting1
Dimethyl Sulfoxide1
Mistletoe/Viscum album Extracts1
Cichoric acid / Chicoric acid1
Cannabichromene1
Tetrahydroxystilbene glucoside1
ferumoxytol1
Arsenic trioxide1
Vitamin A, Retinoic Acid1
carboplatin1
olaparib/LYNPARZA1
Ginseng1
Rapamycin1
High-Ozonide Oil1
Hops (Humulus lupulus)1
Inoscavin A1
Inulin Prebiotic1
Laetrile B17 Amygdalin1
lambertianic acid1
Iron1
magnetic nanoparticles1
Methylsulfonylmethane1
Mushroom Chaga1
Proanthocyanidins1
Rhein1
Rauwolfia serpentina/Indian Snakeroot1
Vorinostat1
Oxaliplatin1
Sulfasalazine1
Scoulerine1
acetazolamide1
Osimertinib1
Adagrasib1
Glutathione1
Tomatine1
Turmerones1
Whole Body Vibration1
xanthohumol1
Zinc Oxide
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:14 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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