TumCD Cancer Research Results
TumCD, Tumor Cell Death: Click to Expand ⟱
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Tumor Cell Death
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
Nor, |
WI38 |
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
PC, |
PANC1 |
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*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↑,
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in-vitro, |
Colon, |
HT29 |
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in-vitro, |
Nor, |
3T3 |
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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
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.
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
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in-vitro, |
Oral, |
NA |
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in-vitro, |
Nor, |
HEK293 |
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in-vitro, |
Nor, |
HaCaT |
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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 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 ⓘ
GSH↓, 1, ROS↑, 1,
Cell Death ⓘ
Apoptosis↑, 1, BAX↑, 1, Bcl-2↓, 1, Casp3↑, 2, Casp7↑, 1, Mcl-1↓, 1, TumCD↓, 5,
Protein Folding & ER Stress ⓘ
CHOP↓, 1, eIF2α↑, 1, ER Stress↑, 1, GRP78/BiP↑, 1, IRE1↑, 1, PERK↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
P53↑, 1,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
E-cadherin↑, 1, Fibronectin↓, 1, TumCMig↓, 1, Vim↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
ATF4↑, 1,
Immune & Inflammatory Signaling ⓘ
p65↓, 1,
Drug Metabolism & Resistance ⓘ
eff↓, 2, selectivity↑, 2,
Total Targets: 30
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1,
Functional Outcomes ⓘ
toxicity∅, 1,
Total Targets: 2
Scientific Paper Hit Count for: TumCD, Tumor Cell Death
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#:619 State#:% Dir#:1
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