TrxR Cancer Research Results

TrxR, Thioredoxin Reductase: Click to Expand ⟱
Source:
Type:
TrxR is an enzyme that reduces Trx, allowing it to perform its reducing functions. It has been shown to have a role in cancer cell metabolism and survival.
TrxR is overexpressed in various types of cancer, including breast, lung, colon, and prostate cancer.

- Part of the thioredoxin system, which regulates reactive oxygen species (ROS).
- TrxR is a major antioxidant systems that maintains the intracellular redox homeostasis.
- Inhibition causes an increase in ROS.
- TrxR is often upregulated in cancer cells to help manage increased oxidative stress, it is seen as a potential therapeutic target. Inhibiting TrxR may result in increased ROS in cancer cells, pushing them toward apoptosis.
- TrxR is a selenoprotein—meaning it incorporates the trace element selenium in the form of the amino acid selenocysteine.

TrxR inhibitors:
-Piperlongumine
-Withania somnifera (Ashwagandha)
-Parthenolide
-EGCG
-Curcumin
-Myricetin
-Gambogic Acid
Scientific Papers found: Click to Expand⟱
2962- PL,    Synthesis of Piperlongumine Analogues and Discovery of Nuclear Factor Erythroid 2‑Related Factor 2 (Nrf2) Activators as Potential Neuroprotective Agents
- in-vitro, Nor, PC12
*GSH↑, compounds 4 and 5 remarkably elevats GSH level and antioxidant enzymes activity (NQO1, Trx, and TrxR).
*NQO1↑,
*Trx↑,
*TrxR↑,
*NRF2↑, revealed that the total Nrf2 expression was slightly upregulated. 4 and 5, have been identified as potent Nrf2 activators with minimal cytotoxicity.
*NRF2⇅, Notably, the cytosolic Nrf2 decreased gradually (Figure 9, middle panel). Coincidently, the amount of Nrf2 in nuclei increased.
*eff↑, Induction of transcription of antioxidant genes via the Nrf2-dependent cytoprotective pathway requires translocation of Nrf2 from cytosol to nucleus.
*BioAv↑, PL could cross the BBB after oral administration
*ROS↓, The elevation of cellular endogenous antioxidant system prevents the accumulation of ROS and thus confers protection against oxidative insults to the cells.

4485- Se,    Selenium stimulates the antitumour immunity: Insights to future research
- Review, NA, NA
*antiOx↑, At nutritional low doses, selenium, depending on its form, may act as an antioxidant, protecting against oxidative stress, supporting cell survival and growth, thus, plays a chemo-preventive role
chemoPv↑,
ROS↑, at supra-nutritional higher pharmacological doses, selenium acts as pro-oxidant inducing redox signalling and cell death
Imm↑, selenium stimulates the immune system against cancer
selenoP↑, anti-oxidant through selenoproteins
*IL2↑, consumption of Se-enriched foods (200 μg per serving for 3 days) increases the levels of interleukin IL-2, IL-4, IL-5, IL-13 and IL-22, indicating an activated Th2-type response
*IL4↑,
*TNF-α↓, taking selenised yeast (300 μg.day−1) downregulates the gene expression of tumour necrosis factor (TNF)α and transforming growth factor (TGF)β; thus, consequently inhibit the epithelial-to-mesenchymal transition (EMT) in non-malignant prostate tissue
*TGF-β↓,
*EMT↓,
Risk↓, immune-enhancing effects of Se may reduce the risk of cancer
*GPx↑, chemo-preventive effects of Se are mainly mediated by the anti-oxidant function of selenoenzymes such as GPxs and TXNRDs [68] because Se supplementation increases both GPx1 and GPx4 activity in humans
*TrxR↑,

4717- Se,    A systematic review of Selenium as a complementary treatment in cancer patients
- Review, Var, NA
*antiOx↑, Selenium, a trace element with antioxidant properties, has been widely studied for its benefits in cancer treatment.
eff↝, clear statement regarding the effectiveness of Se supplementation is not possible
radioP↑, whereas cancer patients with a Se deficiency could profit from a Se supplementation during radio- or chemotherapy.
chemoP↑,
*selenoP↑, Se is crucial for the biosynthesis of selenoproteins and essential enzymes (glutathione peroxidases (GSH-PPX), thioredoxin reductase, and selenoprotein P
*GPx↑,
TrxR↑,
*ROS↓, Glutathione peroxidase, an enzyme within this group, directly neutralizes reactive oxygen species, which can be detrimental to cells.

3663- SFN,    Efficacy of Sulforaphane in Neurodegenerative Diseases
- Review, AD, NA - Review, Park, NA
*antiOx↑, SFN is especially characterized by antioxidant, anti-inflammatory, and anti-apoptotic properties,
*Inflam↓,
*Half-Life↝, SFN in rats reaches the plasma peak in 4 h, with an average half-life of about 2.2 h
*NRF2↑, Nrf2 expression can be regulated by SFN,
*NQO1↑, oxidoreductase 1 (NQO-1), heme oxygenase 1 (HO-1), GSH S-transferase, and thioredoxin reductase, thus counteract the oxidative stress
*HO-1↑, intracellular increase of GSH, as well as HO-1 and NQO-1 activity
*TrxR↑,
*ROS↓,
*TNF-α↓, regulating the levels of inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin (IL) 6, IL-1β, inducible nitric oxide synthetase (iNOS), and cyclooxygenase-2 (COX-2)
*IL1β↓,
*IL6↓,
*iNOS↓,
*COX2↓,
*Aβ↓, SFN inhibited Aβ aggregation, tau hyperphosphorylation, as well as oxidative stress, evaluated through GSH and malondialdehyde (MDA) levels
*GSH↑, reduction of levels of MDA, TNF-α, and IL-1β, as well as by the increase of GSH
*cognitive↑, SFN treatment improved cognitive and locomotor deficits evaluated by Morris water maze and open field test.
*BACE↓, SFN, according to a dose-dependent mechanism, can inhibit BACE-1 and consequently Aβ aggregation
*HSP70/HSPA5↑, SFN increased the levels of co-chaperone of heat shock protein (HSP), C-terminus of HSP 70-interacting protein (CHIP)
*neuroP↑, SFN, through mechanisms that involve Nrf2 activation, can play a protective effect for counteracting the neurodegeneration that occurs in the PD
*ROS↓, SFN treatment has avoided both ROS production and membrane damage.
*BBB↑, SFN protected the integrity of BBB, as shown by tight junction proteins occludin and claudin-5 levels, as well as by the reduction in the expression levels of matrix metallopeptidase 9,
*MMP9↓,

3658- SFN,    Pre-Clinical Neuroprotective Evidences and Plausible Mechanisms of Sulforaphane in Alzheimer’s Disease
- Review, AD, NA
*NRF2↑, Sulforaphane potently induces transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated expression of detoxification, anti-oxidation
*antiOx↑,
*neuroP↑, The study on the neuroprotective effects of sulforaphane began in 2004 with studies showing the protective effects on neurons
*Aβ↓, every other day 10 mg/kg i.p. for 2 months in cortex: (1) reduced the numbers of Aβ plaques/mm2 in cerebral cortex
*BACE↓, reduced BACE1 protein expression
*NQO1↑, increased NQO1 transcript and protein expression
*IL1β↓, decreased IL-1β and TNF-α
*TNF-α↓,
*IL6↓, (1) decreased IL-1β and IL-6 (2) decreased COX-2 and iNOS (3) reduced NF-κB p-p65
*COX2↓,
*iNOS↓,
*NF-kB↓,
*NLRP3↓, reduced NLRP3 inflammasome
*Ca+2↓, decreased intracellular Ca2+ levels
*GSH↑, in brain: (1) increased GSH (2) decreased MDA
*MDA↓,
*ROS↓, (1) decreased ROS and MDA, (2) increased SOD activity
*SOD↑,
*HO-1↑, increased NQO1, HO-1
*TrxR↑, increased HO-1 and TrxR expression
*cognitive↑, ameliorated cognitive deficits
*tau↓, figure 1
*HSP70/HSPA5↑,


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 ⓘ

ROS↑, 1,   selenoP↑, 1,   TrxR↑, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↝, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   chemoPv↑, 1,   radioP↑, 1,   Risk↓, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   GPx↑, 2,   GSH↑, 3,   HO-1↑, 2,   MDA↓, 1,   NQO1↑, 3,   NRF2↑, 3,   NRF2⇅, 1,   ROS↓, 5,   selenoP↑, 1,   SOD↑, 1,   Trx↑, 1,   TrxR↑, 4,  

Cell Death ⓘ

iNOS↓, 2,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,  

Migration ⓘ

Ca+2↓, 1,   MMP9↓, 1,   TGF-β↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 2,   IL2↑, 1,   IL4↑, 1,   IL6↓, 2,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 2,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 2,  

Functional Outcomes ⓘ

cognitive↑, 2,   neuroP↑, 2,  
Total Targets: 38

Scientific Paper Hit Count for: TrxR, Thioredoxin Reductase
2 Selenium
2 Sulforaphane (mainly Broccoli)
1 Piperlongumine
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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