isoquercitrin / ROS Cancer Research Results

ISQ, isoquercitrin: Click to Expand ⟱
Features:

Isoquercitrin - Quercetin-3-O-Glucoside

Alternative Names: Isoquercetin, quercetin-3-O-glucoside, quercetin-3-O-β-D-glucopyranoside, Q3G, IQ

Type: Flavonol glycoside / quercetin glycoside / natural phytochemical

Sources: Naturally present in numerous medicinal plants, fruits, vegetables, and plant-derived foods. Isoquercitrin can also be produced from rutin by enzymatic removal of the rhamnose residue.

Function: Isoquercitrin is a bioactive quercetin glycoside with antioxidant, anti-inflammatory, anticancer, metabolic, and neuroprotective effects. Reported mechanisms include modulation of Nrf2/ARE, NF-κB, JAK/STAT3, PI3K/AKT, MAPK, AMPK, Wnt signaling, oxidative stress, and programmed cell death.

Cancer: Preclinical studies demonstrate inhibition of cancer-cell proliferation, survival, migration, and tumor-associated signaling together with induction of apoptosis and modulation of oxidative stress. Anticancer mechanisms include regulation of Wnt, MAPK, JAK/STAT3, PI3K/AKT, NF-κB, and related signaling pathways.

Alzheimer's Disease: Preclinical studies indicate neuroprotective activity, including improved learning and memory in amyloid-β-induced models and reduction of oxidative and inflammatory neuronal injury.

Isoquercitrin — also called isoquercetin, quercetin-3-O-glucoside, quercetin-3-O-β-D-glucopyranoside, Q3G, IQ, or ISQ, is a naturally occurring flavonol glycoside consisting of quercetin conjugated to glucose at the 3-O position. It is a dietary phytochemical and quercetin derivative found in many fruits, vegetables, medicinal plants, and plant-derived foods; it can also be produced from rutin by enzymatic removal of rhamnose. Isoquercitrin is generally absorbed more efficiently than quercetin aglycone or rutin, but circulating intact isoquercitrin is limited because intestinal and hepatic metabolism rapidly produces quercetin glucuronide, sulfate, methylated, and other metabolites. Enzymatically modified isoquercitrin and α-glycosyl isoquercitrin are related higher-solubility preparations but should not be treated as pharmacokinetically identical to native isoquercitrin.

Primary mechanisms (ranked):

  1. ↓ PI3K/AKT/mTOR survival signaling and ↑ mitochondria-dependent, caspase-mediated apoptosis in several tumor models.
  2. ↑ AMPK signaling with ↓ mTOR/p70S6K activity, producing metabolic stress, autophagy, and apoptosis.
  3. ↓ canonical Wnt/β-catenin transcriptional signaling, including downstream c-Myc, cyclin D1, and survivin in Wnt-dependent tumor models.
  4. ↑ mitochondrial dysfunction and intrinsic apoptosis in susceptible cancer cells, including loss of mitochondrial membrane potential, ↑ Bax/Bcl-2 ratio, PARP cleavage, and caspase activation.
  5. ↑ ROS in selected cancer models, where oxidative stress can function upstream of AMPK activation, autophagy, and apoptosis; this is context-dependent because isoquercitrin is antioxidant in many normal-cell and disease models.
  6. MAPK remodeling, typically ↓ ERK and p38 signaling with ↑ JNK in some cancer models.
  7. ↓ migration, invasion, and EMT-associated phenotypes in several tumor models.
  8. Secondary/context-dependent modulation of JAK/STAT3, NF-κB inflammatory signaling, and NRF2/ARE antioxidant defenses.

Bioavailability / PK relevance: Oral isoquercitrin is absorbed substantially better than rutin and is rapidly processed in the intestine and liver. Human administration of quercetin-3-glucoside produces plasma quercetin-derived conjugates with peak total quercetin concentrations in the low-micromolar range; intact glucoside is essentially absent or present only in very small quantities in plasma. Therefore, systemic biological activity after oral administration is likely mediated substantially by quercetin conjugates and downstream metabolites rather than prolonged exposure to intact isoquercitrin. Enzymatic glycosylation can further improve solubility and systemic exposure, but EMIQ/AGIQ should be distinguished from native isoquercitrin.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 20–200 µM isoquercitrin, whereas human oral exposure produces predominantly quercetin metabolites at substantially lower free/intact isoquercitrin concentrations. Consequently, direct tumor-cell effects demonstrated at tens to hundreds of micromolar intact isoquercitrin may exceed realistically achievable systemic exposure after conventional oral dosing. Lower-micromolar or metabolite-mediated effects have greater translational plausibility. The bladder is a potential special context because urinary exposure to flavonoid metabolites may differ from plasma exposure, but this has not established clinical anticancer efficacy.

Clinical evidence status: Cancer: preclinical only; cell-culture and xenograft evidence exists for hepatocellular, bladder, pancreatic, colorectal, melanoma, osteosarcoma, esophageal and other tumor models, but there is no established anticancer indication or convincing human oncology trial evidence. Human studies of isoquercitrin-related preparations have primarily evaluated cardiovascular, antioxidant, exercise/nutrition, or allergic outcomes rather than cancer. Alzheimer’s disease: preclinical only, with cell and rodent evidence for anti-amyloidogenic, antioxidant, mitochondrial-protective, and cognitive effects; no established human AD efficacy. Regulatory use should not be confused with therapeutic validation: Health Canada lists isoquercitrin as an approved NHP ingredient, while α-glycosyl isoquercitrin has FDA GRAS-notice status for specified food uses; neither status represents approval as a cancer or Alzheimer treatment.

Isoquercitrin Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 PI3K AKT mTOR survival signaling ↓ PI3K
↓ p-AKT
↓ mTOR		 ↔ / context-dependent R/G Reduced survival and anabolic signaling One of the strongest recurring anticancer axes; demonstrated in bladder cancer and melanoma and supported by newer tumor models.
2 AMPK mTOR p70S6K metabolic signaling ↑ p-AMPK
↓ p-mTOR
↓ p70S6K		 ↑ AMPK (context-dependent) R/G Metabolic stress, autophagy, and apoptosis Strong evidence in hepatocellular and bladder cancer models. AMPK activation can be metabolically protective in normal tissue but cytotoxic under tumor stress conditions.
3 Wnt β-catenin transcription ↓ Wnt transcription
↓ c-Myc
↓ Cyclin D1
↓ Survivin		 ↔ / model-dependent R/G Reduced proliferation and survival Direct functional inhibition of canonical Wnt signaling has been demonstrated in colorectal cancer. Osteosarcoma studies also implicate β-catenin suppression. Direction is tissue-dependent outside cancer.
4 Mitochondrial apoptosis ↑ Bax/Bcl-2 ratio
↓ mitochondrial membrane potential
↑ caspase-9
↑ caspase-3
↑ PARP cleavage		 ↔ / ↓ apoptosis under oxidative injury R/G Intrinsic programmed cell death Frequently observed tumor phenotype. Selectivity is model-dependent; isoquercitrin can instead protect normal cells from mitochondrial oxidative injury.
5 Autophagy ↑ (excessive or pro-death; model-dependent) ↑ / ↔ (stress-dependent) R/G Autophagic stress contributing to apoptosis In HCC, autophagy inhibition reduces isoquercitrin-induced apoptosis, supporting a functional pro-death role. Similar excessive autophagy is reported in ESCC.
6 Reactive oxygen species stress ↑ (context-dependent) ↓ (commonly antioxidant) P/R Redox-mediated tumor stress In T24 bladder cancer cells ROS rises upstream of AMPK and apoptosis. In normal or oxidatively injured cells isoquercitrin commonly lowers ROS, indicating potentially useful redox selectivity but not a universal tumor-specific mechanism.
7 MAPK ERK JNK p38 signaling ↓ ERK
↓ p38
↑ JNK (model-dependent)		 ↓ stress MAPK activation in injury models R/G Growth suppression and apoptotic signaling Reported in liver and pancreatic cancer models. Direction is stimulus- and tissue-dependent, particularly in normal cells.
8 Cell cycle progression ↓ proliferation
↑ G1 or sub-G1 arrest		 ↔ at lower exposures G Growth arrest G1 arrest is reported in liver, pancreatic, and bladder models; sub-G1 accumulation accompanies apoptosis in melanoma.
9 Migration invasion and EMT ↓ migration
↓ invasion
↓ mesenchymal phenotype		 ↔ G Reduced metastatic phenotype Observed in osteosarcoma and esophageal cancer models and linked partly to Wnt and AKT/mTOR suppression.
10 JAK STAT3 signaling ↓ STAT3 (model-dependent) ↓ JAK2 STAT3 during inflammatory injury R/G Reduced survival and inflammatory transcription Evidence exists in bladder cancer and non-cancer inflammatory models, but this is less consistently established than PI3K/AKT, AMPK, or Wnt signaling.
11 NF-κB inflammatory signaling ↓ (context-dependent) ↓ inflammatory activation R/G Anti-inflammatory signaling Supported broadly in isoquercitrin pharmacology but is better established as an anti-inflammatory mechanism than as a primary tumor-killing mechanism.
12 NRF2 ARE antioxidant response ↑ / context-dependent ↑ NRF2 antioxidant defense R/G Secondary cytoprotective redox regulation Important in normal-tissue protection and oxidative-stress models. NRF2 activation can theoretically protect malignant cells, so it should not be represented as an unqualified anticancer mechanism.
13 Glycolytic and lipid metabolism ↓ / dysregulated (model-dependent) ↔ / metabolically adaptive R/G Metabolic disruption Metabolomic analysis in bladder cancer indicates altered anaerobic glycolysis and lipid synthesis downstream of ROS and AMPK. Evidence is presently tumor-model specific.
14 Clinical Translation Constraint ↓ effective systemic target exposure Extensive first-pass metabolism G Exposure and evidence limitation Many anticancer studies use 20–200 µM intact isoquercitrin. Human plasma after oral quercetin-3-glucoside contains predominantly glucuronidated and sulfated quercetin metabolites rather than intact isoquercitrin, making direct extrapolation from high-concentration cell studies uncertain. No established oncology efficacy in humans.

TSF: P: 0–30 min     R: 30 min–3 hr     G: >3 hr



Alzheimer’s disease relevance: Isoquercitrin has meaningful but entirely preclinical AD-related evidence. Reported effects include direct inhibition of β- and γ-secretase activity, ↓ Aβ aggregation with enhanced disaggregation in cell-free systems, ↓ amyloidogenic proteins including β-secretase and presenilins in animal models, ↓ neuronal oxidative stress, preservation of mitochondrial function, ↓ apoptosis, and improved learning and memory in Aβ- and streptozotocin-based rodent models. These findings support an anti-amyloidogenic and neuroprotective research classification, but there is currently no convincing human clinical evidence demonstrating prevention or treatment of Alzheimer’s disease.

Translation constraint: Most AD evidence uses experimental Aβ25-35 injection, streptozotocin, cell-based amyloid systems, or other simplified models that do not reproduce the full biology of sporadic human AD. Oral metabolism also means that brain exposure to intact isoquercitrin is uncertain and circulating quercetin metabolites may contribute substantially to any systemic effect.

Isoquercitrin Alzheimer-Relevant Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Amyloid β production and aggregation ↓ Aβ formation
↓ aggregation
↑ disaggregation		 Reduced amyloid burden Cell-free and cellular studies report direct anti-amyloidogenic activity; rodent studies show decreased brain amyloidosis-related proteins.
2 β-secretase ↓ Reduced amyloidogenic APP processing Direct enzyme inhibition has been reported in vitro, and β-secretase expression is reduced in Aβ/HFD animal models.
3 γ-secretase and presenilins ↓ γ-secretase activity
↓ PS1
↓ PS2		 Reduced Aβ-generating processing Secretase inhibition is demonstrated in biochemical assays; reduced presenilin expression has been reported in mouse brain.
4 Neuronal oxidative stress ↓ ROS
↓ lipid peroxidation
↓ nitric oxide stress		 Neuroprotection Strong recurring mechanism across Aβ- and STZ-based experimental models.
5 Mitochondrial function ↑ preservation Reduced neuronal energy failure Isoquercitrin attenuates STZ-induced mitochondrial dysfunction and neuronal cytotoxicity.
6 Neuronal apoptosis ↓ caspase activation
↓ apoptosis		 Improved neuronal survival Opposite direction to many cancer models, illustrating disease- and stress-dependent modulation.
7 Proteasome function ↑ 20S chymotrypsin-like activity Improved damaged-protein clearance Reported in oxidative-stress APP cellular systems; translational importance remains uncertain.
8 Cognition and memory ↑ Improved behavioral performance Improvement has been demonstrated in Aβ/HFD mouse and STZ rat models but not yet in human AD trials.
9 Clinical Translation Constraint Preclinical only Uncertain human efficacy No established human AD efficacy; model validity, brain exposure, metabolism, and effective dose remain major uncertainties.


ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
7843- ISQ,    In vitro response of human ovarian cancer cells to dietary bioflavonoid isoquercitrin
- in-vitro, Ovarian, OVCAR-3
tumCV∅, ROS↓, ROS↑,
7793- ISQ,    Apoptosis triggered by isoquercitrin in bladder cancer cells by activating the AMPK-activated protein kinase pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, ROS↑, AMPK↑, Glycolysis↓, p‑PI3K↓, p‑Akt↓, Casp↑, mTOR↓, ACC↓, FASN↓,
7797- ISQ,    Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway
- vitro+vivo, ESCC, KYSE-510 - in-vitro, ESCC, KYSE450
TumCG↓, Apoptosis↓, Casp↑, Bcl-2↓, EMT↓, TumAuto↑, ROS↑, Akt↓, PI3K↓, Catalase↓, SOD1↓, SOD2↓, eff↓,
7810- ISQ,    Isoquercitrin Inhibits Lung Cancer Cell Growth Through Triggering Pyroptosis and Ferroptosis
- vitro+vivo, Lung, A549 - in-vitro, Nor, BEAS-2B
tumCV↓, selectivity↑, Apoptosis↑, NLRP3↑, Pyro↑, Ferroptosis↑, ROS↑, eff↓, Dose↝, TumCG↓,
7812- ISQ,    Isoquercitrin promotes ferroptosis and oxidative stress in nasopharyngeal carcinoma via the AMPK/NF-κB pathway
- vitro+vivo, NPC, CNE1 - in-vitro, NPC, HNE1
tumCV↓, TumCP↓, ROS↑, lipid-P↑, NF-kB↓, MAPK↓, IL1β↓, TumCG↓, lipid-P↓, Ferroptosis↓, eff↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   Ferroptosis↓, 1,   Ferroptosis↑, 1,   lipid-P↓, 1,   lipid-P↑, 1,   ROS↓, 1,   ROS↑, 5,   SOD1↓, 1,   SOD2↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↓, 1,   AMPK↑, 1,   FASN↓, 1,   Glycolysis↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Casp↑, 2,   Ferroptosis↓, 1,   Ferroptosis↑, 1,   MAPK↓, 1,   Pyro↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 3,   tumCV∅, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   mTOR↓, 1,   PI3K↓, 1,   p‑PI3K↓, 1,   TumCG↓, 3,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   NF-kB↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,   eff↓, 3,   selectivity↑, 1,  
Total Targets: 38

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
5 isoquercitrin
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#:455  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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