TumCD Cancer Research Results

TumCD, Tumor Cell Death: Click to Expand ⟱
Source:
Type:
Tumor Cell Death
Scientific Papers found: Click to Expand⟱
4541- AgNPs,  RosA,    Eco-friendly synthesis of silver nanoparticles: multifaceted antioxidant, antidiabetic, anticancer, and antimicrobial activities
- in-vitro, Nor, WI38 - in-vitro, BC, MDA-MB-231 - in-vitro, PC, PANC1
*antiOx↑, Potent antioxidant activity was observed with an EC₅₀ of 7.81 µg mL⁻1, close to ascorbic acid (3.27 µg mL⁻1).
TumCD↓, Ag-NPs showed selective cytotoxicity against MDA and PANC-1 cells (IC₅₀: 177.2 and 115.3 µg mL⁻1), with lower toxicity toward Vero and Wi38 normal cells (IC₅₀: 233 and 207 µg mL⁻1).
selectivity↑,

6214- CUR,    Curcumin Nanoparticles-related Non-invasive Tumor Therapy, and Cardiotoxicity Relieve
TumCD↓, Curcumin plays the antitumor effect by directly promoting tumor cell death and reducing tumor cells' invasive ability.
TumCI↓,
*Inflam↓, curcumin has many pharmacological effects, such as anti-inflammation, antioxidation, antitumor, etc.
*antiOx↓,
*AntiTum↓,
NF-kB↓, Curcumin exerts the therapeutic effect mainly by inhibiting the nuclear factor-κB (NF-κB) signal pathway, inhibiting the production of cyclooxygenase-2 (COX-2),
COX2↓,
Casp9↓, promoting the expression of caspase-9, and directly inducing reactive oxygen species (ROS) production in tumor cells.
ROS↑, Curcumin can induce lethal levels of reactive oxygen species (ROS) in tumors
BioAv↑, Curcumin nanoparticles can solve curcumin's shortcomings, such as poor water solubility and high metabolic rate, and can be effectively used in antitumor therapy.
RadioS↑, Figure 1, Curcumin Increases Radiosensitivity of Tumor
ChemoSen↑,
Imm↑,
PhotoS↑, Curcumin Mediates the Antitumor Effect of PDT
sonoS↑, Curcumin Mediates the Antitumor Effect of SDT
5LO↓, down-regulating the activities of cyclooxygenase-2 (COX-2), lipoxygenase (LOX), inducible nitric oxide synthase (iNOS) and so on, reducing the production of proinflammatory cytokines such as IL-2, tumor necrotic factor-α (TNF-α),
iNOS↓,
IL2↓,
TNF-α↓,
Casp9↑, activating intracellular caspase-9 and caspase-3, reducing the expression of p53, inhibiting Bcl2, and promoting the expression of Bax and down-regulating the proportion of Bcl2/Bax
Casp3↑,
Bcl-2↓,
BAX↑,
Apoptosis↑, promote apoptosis by activating caspase-4 and stimulating the Endoplasmic reticulum (ER) stress pathway and mitochondria stress pathway in tumor cells [
ER Stress↑,
cycD1/CCND1↓, It reduces the expression of cyclin D1, cyclin kinase-dependent kinase 2 (CDK2), cdc2/cyclin B complex, and other cell cycle-related proteins,
CDK2↓,
CycB/CCNB1↓,
TumCCA↑, blocks tumor cells from G1 / S phase and G2 / M phase, thus exerting an antitumor effect
MMPs↓, curcumin inhibits tumor invasion and metastasis by inhibiting NF-κB and other signaling pathways, such as chemokine and matrix metalloproteinases (MMPs)
*radioP↑, Curcumin can effectively treat and prevent radiation adverse reactions such as radiation dermatitis and radiation pneumonia by reducing the expression of inflammatory factors such as fibrotic cytokines, TNF-α, and IL-1, inhibiting NF-κB signal pathwa
chemoP↑, Protective Effect of Curcumin on Side Effects of Chemotherapy
hepatoP↑, urcumin alleviates the hepatotoxicity caused by chemotherapy through anti-inflammation and antioxidation, reducing the level of liver fibrosis and blood lipids [
cardioP↑, Using curcumin to reduce the cardiotoxicity of chemotherapy can improve the therapeutic effect of tumors and patients' prognosis and quality of life.
eff↑, Curcumin Enhances the Therapeutic Effect of Immunotherapy
PhotoS↑, it has the potential to be a new photosensitizer
eff↑, Curcumin nanoparticles with functions of relieving hypoxia and consuming GSH could improve the ability of curcumin to induce ROS and promote ROS- mediated tumor cell death
ROS↑,
GSH↓,

3208- EGCG,    Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2α/ATF4 and IRE1α
- in-vitro, Colon, HT29 - in-vitro, Nor, 3T3
TumCD↓, EGCG treatment was toxic to the HT-29 cell line
ER Stress↑, EGCG induced ER stress in HT-29 by upregulating immunoglobulin-binding (BiP), PKR-like endoplasmic reticulum kinase (PERK), phosphorylation of eukaryotic initiation factor 2 alpha subunit (eIF2α), activating transcription 4 (ATF4), and IRE1α
GRP78/BiP↑,
PERK↑,
eIF2α↑,
ATF4↑,
IRE1↑,
Apoptosis↑, Apoptosis was induced in HT-29 cells after the EGCG treatment, as shown by the Caspase 3/7 activity.
Casp3↑,
Casp7↑,
Wnt↓, (CRC) via suppression of the Wnt/β-catenin pathway
β-catenin/ZEB1↓,
*toxicity∅, This embryonic fibroblast cell line (3T3) has shown that the EGCG was not toxic to normal healthy cells, given the treatment at any concentration even at the highest concentration of EGCG (1000 μM).
UPR↑, ER stress is induced by EGCG and activates UPR proteins

5931- EGCG,  BTZ,    EGCG antagonizes Bortezomib cytotoxicity in prostate cancer cells by an autophagic mechanism
- in-vitro, Pca, PC3
TumAuto↑, EGCG antagonizes BZM toxicity by exacerbating the activation of autophagy, which in turn mitigates ER stress and reduces CHOP up-regulation, finally protecting PC3 cells from cell death.
CHOP↓,
TumCD↓,
eff↓, These results demonstrate that EGCG reduces BZM but not MG132 cytotoxicity in PC3 cells.

4953- PEITC,    PEITC: a natural compound effective in killing primary leukemia cells and overcoming drug resistance
- in-vitro, CLL, NA
ROS↑, Based on the recent observations that β-phenylethyl isothiocyanate (PEITC) causes significant ROS increase in cancer cells by disabling the GSH antioxidant system
GSH↓,
TumCD↓, PEITC effectively killed both F-ara-A sensitive (n=7, IC50 range: 0.5-10 µM) and resistant (n=4, IC50>50 µM,) CLL cells, with similar IC50 values of 4-8 µM.
eff↓, Antioxidant N-acetylcysteine (NAC) suppressed PEITC-induced ROS accumulation and cell death, suggesting that this compound killed CLL cells through ROS-mediated mechanism.
Mcl-1↓, PEITC treatment led to a significant decrease in MCL-1 protein without detectable change in BCL-2 protein level.
Casp3↑, PEITC induced caspase-3 activation

1821- VitK3,    Menadione (Vitamin K3) induces apoptosis of human oral cancer cells and reduces their metastatic potential by modulating the expression of epithelial to mesenchymal transition markers and inhibiting migration
- in-vitro, Oral, NA - in-vitro, Nor, HEK293 - in-vitro, Nor, HaCaT
selectivity↑, menadione is more cytotoxic to SAS (oral squamous carcinoma) cells but not to non-tumorigenic HEK293 and HaCaT cells.
TumCD↓,
BAX↑, increased the expression of pro-apoptotic proteins, Bax and p53
P53↑,
Bcl-2↓, concurrent decrease in anti-apoptotic proteins, Bcl-2 and p65
p65↓,
E-cadherin↑, Menadione induced the expression of E-cadherin
EMT↓, but reduced the expression of EMT markers, vimentin and fibronectin
Vim↓,
Fibronectin↓,
TumCG↓, Menadione also inhibited anchorage independent growth and migration in SAS cells.
TumCMig↓,


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 2,   ROS↑, 3,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 3,   Casp7↑, 1,   Casp9↓, 1,   Casp9↑, 1,   iNOS↓, 1,   Mcl-1↓, 1,   TumCD↓, 6,  

Transcription & Epigenetics ⓘ

PhotoS↑, 2,   sonoS↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   eIF2α↑, 1,   ER Stress↑, 2,   GRP78/BiP↑, 1,   IRE1↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

5LO↓, 1,   E-cadherin↑, 1,   Fibronectin↓, 1,   MMPs↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL2↓, 1,   Imm↑, 1,   NF-kB↓, 1,   p65↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   eff↓, 2,   eff↑, 2,   RadioS↑, 1,   selectivity↑, 2,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,  
Total Targets: 54

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

AntiTum↓, 1,   radioP↑, 1,   toxicity∅, 1,  
Total Targets: 6

Scientific Paper Hit Count for: TumCD, Tumor Cell Death
2 EGCG (Epigallocatechin Gallate)
1 Silver-NanoParticles
1 Rosmarinic acid
1 Curcumin
1 Bortezomib
1 Phenethyl isothiocyanate
1 VitK3,menadione
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

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