TrxR2 Cancer Research Results

TrxR2, thioredoxin reductase-mitochondrial: Click to Expand ⟱
Source:
Type:
TrxR2 is a mitochondrial selenoprotein that reduces oxidized Trx2, thereby preserving a reduced environment within the mitochondria.
• By maintaining mitochondrial redox homeostasis, TrxR2 contributes to cell survival, protects against oxidative stress, and helps regulate apoptosis.
• Its activity is especially critical in rapidly proliferating cells, such as cancer cells, which often experience elevated levels of reactive oxygen species (ROS).

-In various cancers—such as breast, lung, and colorectal cancers—upregulation of TrxR2 has been linked to enhanced cell survival, resistance to oxidative stress, and, in some studies, poorer clinical outcomes.
Scientific Papers found: Click to Expand⟱
5461- AF,    Dual inhibition of thioredoxin reductase and proteasome is required for auranofin-induced paraptosis in breast cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
Paraptosis↑, We show here that 4~5 µM AF induces paraptosis, a non-apoptotic cell death mode characterized by dilation of the endoplasmic reticulum (ER) and mitochondria, in breast cancer cells.
ER Stress↑,
TrxR↓, covalent inhibition of thioredoxin reductase (TrxR)
selectivity↑, subtoxic doses of AF and Bz induced paraptosis selectively in breast cancer cells, sparing non-transformed MCF10A cells
toxicity↝, whereas 4~5 μM AF killed both cancer and MCF10A cells
ROS↑, We found that treatment with 5 μM AF very weakly and transiently increased ROS levels at 2~4 h and then again at 24 h
mt-TrxR1↓, AF inhibits cytosolic and mitochondrial TrxR (TrxR1 and TrxR2), two selenoenzymes for the Trx pathway [3]
mt-TrxR2↓,

1984- PTL,    Targeting Thioredoxin Reductase by Parthenolide Contributes to Inducing Apoptosis of HeLa Cells
- in-vitro, Cerv, HeLa
AntiCan↑, PTL demonstrates potent anticancer efficacy in numerous types of malignant cells,
TrxR1↓, PTL interacts with both cytosolic thioredoxin reductase (TrxR1) and mitochondrial thioredoxin reductase (TrxR2)
TrxR2↓,
ROS↑, elicit reactive oxygen species-mediated apoptosis in HeLa cells
Apoptosis↑,
eff↓, blocked by pretreatment of the cells with NAC
eff↑, depletion of cellular GSH by pretreatment of the cells with BSO enhances the cytotoxicity of PTL


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,   TrxR↓, 1,   TrxR1↓, 1,   mt-TrxR1↓, 1,   TrxR2↓, 1,   mt-TrxR2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Paraptosis↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   toxicity↝, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TrxR2, thioredoxin reductase-mitochondrial
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#:1222  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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