TrxR1 Cancer Research Results

TrxR1, thioredoxin reductase 1: Click to Expand ⟱
Source:
Type:
TrxR1 or TXNRD1 (Thioredoxin Reductase 1)
Redox Control, Stress Tolerance, and Therapy Resistance
• Many studies have found that an elevated expression of TrxR1 in breast tumors, NSCLC, HCC correlates with increased tumor aggressiveness and a poorer prognosis.
-TrxR1 expression was elevated by >50 fold in FaDu and HeLa cells, and by >20 fold in SCC-1 compared to either MSK-Leuk1 or keratinocytes.

High TXNRD1 expression often associates with:
-Advanced stage
-Therapy resistance
-Reduced survival

TrxR1 Inhibition
-Collapses redox control
-Causes rapid ROS accumulation
-Triggers apoptosis, especially in high-stress tumors


Scientific Papers found: Click to Expand⟱
2873- HNK,    Honokiol Alleviates Oxidative Stress-Induced Neurotoxicity via Activation of Nrf2
- in-vitro, Nor, PC12
*neuroP↑, multiple pharmacological functions, including neuroprotection.
*GSH↑, Hon attenuates the H2O2- or 6-hydroxydopamine (6-OHDA)-induced apoptosis of PC12 cells by increasing the glutathione level
*HO-1↑, and upregulating a multitude of cytoprotective proteins, including heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, thioredoxin 1, and thioredoxin reductase 1.
*NADPH↑,
*Trx1↑,
*TrxR1↑,
*NRF2↑, Hon promotes transcription factor Nrf2 nuclear translocation and activation.
*ROS↓, Hon is promising for further development as a therapeutic drug against oxidative stress-related neurodegenerative disorders. Inhibition of ROS accumulation
*antiOx↑, Upregulation of antioxidant species in PC12 cells
*BBB↑, Hon has the ability to cross the BBB
Dose↓, We demonstrated here that Hon, at the concentration as low as 5 μM, significantly rescues the cells from H2O2- or 6-OHDA-induced oxidative damage

2902- HNK,  Rad,    Honokiol Mitigates Ionizing Radiation-Induced Injury by Maintaining the Redox Balance of the TrxR/Trx System
- in-vitro, Nor, BEAS-2B
*TrxR1↑, HKL pre-exposure significantly increased the expressions of TrxR1 and Trx proteins in general, in particular at doses ranging between 0.05 and 5 µM HKL
*Trx↑,
*radioP↑, Overall, the findings presented here demonstrate that HKL has the potential to be a novel radioprotector capable of cellular protection against radiation-induced injuries
*ROS↓, Compared to the IR group, there was a significant decrease in the ROS levels of the HKL+IR treated group

5785- MET,    Metformin improves healthspan and lifespan in mice
- in-vivo, Nor, NA
*AntiDiabetic↑, Metformin is a drug commonly prescribed to treat patients with type 2 diabetes.
*AntiAge↑, Here we show that long-term treatment with metformin (0.1% w/w in diet) starting at middle age extends healthspan and lifespan in male mice
*toxicity⇅, while a higher dose (1% w/w) was toxic.
*CRM↑, The effects of metformin resembled to some extent the effects of caloric restriction, even though food intake was increased.
*Strength↑, Treatment with metformin mimics some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced LDL and cholesterol levels without a decrease in caloric intake
*LDL↓,
*AMPK↑, metformin increases AMP-activated protein kinase activity and increases antioxidant protection, resulting in reductions in both oxidative damage accumulation and chronic inflammation
*TAC↑,
*ROS↓, consistent with decreased oxidative stress damage in the liver of metformin-treated mice
*Inflam↓, Metformin inhibits chronic inflammation
Risk↓, metformin treatment has been associated with reduced risk of cancer4 and cardiovascular disease
*cardioP↑,
*ALAT↓, Ala aminotransferase (U/L) 90 ± 58 64 ± 29
*NRF2↑, The increase in Nrf2/ARE reporter activity occurred with an ED50 of ~1.5 mM metformin without reduction in cell survival
*SOD2↑, 0.1% metformin contributed to an increase in the level of antioxidant and stress response proteins, including SOD2, TrxR1, NQO1 and NQO2
*TrxR1↑,
*NQO1↑,
*NQO2↑,

4736- Se,  SFN,    Synergy between sulforaphane and selenium in protection against oxidative damage in colonic CCD841 cells
- in-vitro, Nor, CCD841
*TrxR1↑, Treatment of cells with SFN and Se significantly induced TrxR-1 expression.
*H2O2↓, Pretreatment of cells with SFN protects against H2O2-induced cell death; this protection was enhanced by cotreatment with Se.
*NRF2↑, SFN activates the Nrf2 signaling pathway and protects against H2O2-mediated oxidative damage in normal colonic cells.


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Drug Metabolism & Resistance ⓘ

Dose↓, 1,  

Functional Outcomes ⓘ

Risk↓, 1,  
Total Targets: 2

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   H2O2↓, 1,   HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 3,   ROS↓, 3,   SOD2↑, 1,   TAC↑, 1,   Trx↑, 1,   Trx1↑, 1,   TrxR1↑, 4,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 1,   CRM↑, 1,   LDL↓, 1,   NADPH↑, 1,  

Protein Folding & ER Stress ⓘ

NQO2↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 1,   neuroP↑, 1,   radioP↑, 1,   Strength↑, 1,   toxicity⇅, 1,  
Total Targets: 28

Scientific Paper Hit Count for: TrxR1, thioredoxin reductase 1
2 Honokiol
1 Radiotherapy/Radiation
1 Metformin
1 Selenium
1 Sulforaphane (mainly Broccoli)
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#:1207  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page