Trx Cancer Research Results

Trx, Thioredoxin: Click to Expand ⟱

Source:

Type: protein

Trx is a small protein that acts as a reducing agent, donating electrons to reduce oxidized proteins and other molecules.
Trx is overexpressed in various types of cancer, including breast, lung, colon, and prostate cancer.

- Cytosolic thioredoxin (TRX-1) and mitochondrial thioredoxin (TRX-2).

- Thioredoxin is a pivotal redox regulator that protects cells from oxidative stress and supports survival and proliferation.

- There is interest in combining thioredoxin inhibitors with conventional chemotherapy or radiotherapy to sensitize tumors to oxidative stress and improve treatment efficacy.

Scientific Papers found: Click to Expand⟱

2394-

CAP,

Capsaicin acts as a novel NRF2 agonist to suppress ethanol induced gastric mucosa oxidative damage by directly disrupting the KEAP1-NRF2 interaction

in-vitro,

Nor,

GES-1

(0, 2, and 8 μM)

*mtDam↓, CAP ameliorated mitochondrial damage, facilitated the nuclear translocation of NRF2, thereby promoting the expression of downstream antioxidant response elements, HO-1, Trx, GSS and NQO1 in GES-1 cells.
*NRF2↑,
*HO-1↑,
*Trx↑,
*GSS↑,
*NQO1↑,
*Keap1↓, CAP could directly bind to KEAP1 and inhibit the interaction between KEAP1 and NRF2.
*ROS↓, Capsaicin protects GES-1 from oxidative stress
*PKM2↓, Previous studies have demonstrated that CAP can directly bind to and inhibit the activity of PKM2 and LDHA, subsequently attenuating inflammatory response
*LDHA↓,
*Inflam↓,

4513-

GLA,

Antineoplastic Effects of Gamma Linolenic Acid on Hepatocellular Carcinoma Cell Lines

in-vitro,

Liver,

HUH7

TumCP↓, GLA treatment significantly reduced cell proliferation, generated ROS, and induced apoptosis.
ROS↑, The ROS levels were increased 3.4-fold by 3 h exposure to GLA compared to the control
Apoptosis↑,
HO-1↑, antioxidant proteins to be upregulated: heme oxygenase-1 (HO-1), aldo-keto reductase 1 family C1 (AKR1C1), C4 (AKR1C4), and thioredoxin (Trx).
Trx↑,
lipid-P↑, GLA treatment has induced cell growth inhibition, ROS generation including lipid peroxidation, and HO-1 production for antioxidant protection against oxidative stress caused by GLA in Huh7 cells.
eff↓, Our study showed that the cytotoxic effect of GLA was almost blocked when the Huh7 cells were supplemented with Vitamin E in addition to GLA.
MMP↓, decreased mitochondrial membrane potential was observed in our study.
DNAdam↑, we observed DNA fragmentation in Huh7 cells under GLA expose.
selectivity↑, We had observed that no cytotoxicity of primary cultured hepatocytes from rat liver was observed in a concentration of GLA of 250 µM

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

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.

4827-

QC,

CUR,

Synthetic Pathways and the Therapeutic Potential of Quercetin and Curcumin

Review,

Var,

*AntiCan↑, their anti-cancer effects, but also with regard to their anti-diabetic, anti-obesity, anti-inflammatory, and anti-bacterial actions.
*Inflam↓,
*Bacteria↓,
*AntiDiabetic↑,
*ROS↓, suppression of ROS formation via the inhibition of the enzyme activities involved in their production, or via scavenging ROS directly by acting as hydrogen donors; the chelation of the metal ions that induce ROS production;
*SOD↑, quercetin can eliminate free radicals and help maintain a stable redox state in cells by increasing anti-oxidant enzymes, such as superoxide dismutase (SOD), and catalase expressions, as well as the level of reduced glutathione (GSH)
*Catalase↑,
*GSH↑,
*NRF2↑, Quercetin can protect human granulosa cells from oxidative stress by inducing Nrf2 expression at both the gene and protein levels, which in turn induces the anti-oxidant thioredoxin (Trx) system.
*Trx↑,
*IronCh↑, pure curcumin, a metal chelator, directly removes ROS and regulates numerous enzymes.
*MDA↑, It has the potential to reduce the concentration of malondialdehyde (MDA) in serum and increase the total anti-oxidant potential
cycD1/CCND1↓, Cyclin D1 expression was significantly decreased in quercetin-treated ovarian SKOV-3 cells, but not in cisplatin (CDDP)-resistant SKOV3/CDDP cells.
PI3K↓, The levels of PI3K and phospho-Akt were decreased in curcumin-treated SKOV3 cells, which in turn increased caspase-3 and Bax levels.
Casp3↑,
BAX↑,
ChemoSen↑, Curcumin enhanced the efficacy of chemotherapy in colorectal cancer cells.
ROS↑, suggesting that quercetin-induced cytotoxicity and autophagy were initiated by the generation of ROS
eff↑, quercetin or curcumin with chemotherapeutic agents, as shown below, considerably enhances the antitumor potencies of doxorubicin (DOX) and cisplatin.
MMP↓, The synergistic treatment with curcumin and quercetin inhibited the cell proliferation associated with the loss of mitochondrial membrane potential (ΔΨm), the release of cytochrome c, a decrease in AKT and ERK phosphorylation in MGC803 human gastric
Cyt‑c↑,
Akt↓,
ERK↓,

3026-

RosA,

Modulatory Effect of Rosmarinic Acid on H2O2-Induced Adaptive Glycolytic Response in Dermal Fibroblasts

in-vitro,

Nor,

0–100 μM

 dermal fibroblasts

*ROS↓, H2O2 caused a significant ROS increase in the cells, and pre-treatment with rosmarinic acid (5–50 µM) decreased ROS significantly in the presence of glutathione
*ATP↑, The rosmarinic acid also recovered intracellular ATP and decreased NADPH production via the pentose phosphate pathway.
*NADPH↓,
*HK2↓, (HK-2), phosphofructokinase-2 (PFK-2), and lactate dehydrogenase A (LDHA), were downregulated in cells treated with rosmarinic acid
*PFK2↓,
*LDHA↓,
*GSR↑, GSR), glutathione peroxidase-1 (GPx-1), and peroxiredoxin-1 (Prx-1) and redox protein thioredoxin-1 (Trx-1) were upregulated in treated cells compared to control cells.
*GPx↑,
*Prx↑,
*Trx↑,
*antiOx↑, To sum up, the rosmarinic acid could be used as an antioxidant against H2O2-induced adaptive responses in fibroblasts by modulating glucose metabolism, glycolytic genes, and GSH production.
*GSH↑, The pre-treatment of rosmarinic acid could raise intracellular GSH to protect cells from ROS
*ROS↓, rosmarinic acid pre-treatment reduced the amount of ROS in the fibroblasts upon the addition of H2O2
*GlucoseCon↓, both compounds also decreased glucose consumption and lactate production
*lactateProd↓,
*Glycolysis↝, The results indicated that rosmarinic acid is able to shape cellular glucose utilization, glycolysis, and GSH.
*ATP↑, The rosmarinic acid also recovered intracellular ATP and decreased NADPH production via the pentose phosphate pathway.
*NADPH↓,
*PPP↓,

4199-

SFN,

Sulforaphane and Brain Health: From Pathways of Action to Effects on Specific Disorders

Review,

AD,

Review,

Park,

*BBB↑, SF is able to cross the blood–brain barrier as well as to protect it
*BDNF↑, SF can protect against neuronal cell death by inhibiting apoptosis, by upregulating brain-derived neurotrophic factor (BDNF) it can enhance neuronal function and plasticity, and support neurogenesis.
*neuroG↑,
*NRF2↑, , Nrf2 inducers like SF that have no direct redox activity are often referred to as “indirect antioxidants”
*HO-1↑, (NQO1) (HO-1 or HMOX), as well as (Cat), (SOD), (Prx), (HSP), glutathione S-transferases (GST), thioredoxin reductase (Trx), glutathione synthetase (GS), glutathione peroxidases (GPx) and glutathione reductase in the brain
*Catalase↑,
*SOD↑,
*HSPs↑, It enhances the expression of HSP70, HSP90, and HSP40 in normal human fibroblasts
*GSTs↑,
*Trx↑,
*GPx↑,
*GSR↑,
*GSH↑, ability of SF to upregulate GSH in the brain is critical for antioxidant protection in youth but may become even more important with age.
*NQO1↑, SF administration to astrocytes increased NQO1 concentrations and protected against oxygen and glucose-induced astrocyte cell death
*GutMicro↑, the fact that SF modulates microbiome composition
*Inflam↓, reduces inflammation and enhances gut barrier integrity,
*neuroP↑, The effect of SF on the gut microbiome may also affect the production of short-chain fatty acids (SCFA) like butyrate, which have neuroprotective effects

3648-

SIL,

Silymarin/Silybin and Chronic Liver Disease: A Marriage of Many Years

Review,

NA,

*antiOx↑, antioxidant, anti-inflammatory and antifibrotic power
*Inflam↓,
*lipid-P↓, reduce both lipid peroxidation and cellular necrosis.
*necrosis↓,
*hepatoP↑, silybin use in chronic liver diseases, cirrhosis and hepatocellular carcinoma.
*IL1↓, figure 1
*IL6↓,
*TNF-α↓,
*IFN-γ↓,
MAPK↓,
Apoptosis↑,
Cyt‑c↑,
Casp3↑,
Casp9↑,
*PPARγ↑,
*GLUT4↑,
*HSPs↓,
*HSP27↑,
*Trx↑,
*SIRT1↑,
*ALAT↓, as well as prevent ALT increase, Glutathione (GSH) decrease, lipid peroxidation and TNF-α increase
*GSH↑,
*lipid-P↓,
*TNF-α↓,
TumCG↓, silybin significantly reduces HuH7, HepG2, Hep3B, and PLC/PRF/5 human hepatoma cells growth by increasing cyclin-dependent kinase inhibitor p21 and p27/cyclin-dependent kinase (CDK) 4 complexes, by reducing retinoblastoma protein (Rb)-phosphorylatio
P21↑,
CDK4↑,

3302-

SIL,

Protective effects of silymarin in glioblastoma cancer cells through redox system regulation

in-vitro,

GBM,

U87MG

264.6 μM

NRF2↑, The expression level of Nrf2 and HO-1 and glutaredoxin and thioredoxin enzymes were checked by real-time PCR method, and the expression level increased significantly after treatment.
HO-1↑,
Trx↑,
antiOx↑, Our findings suggest that silymarin may exert its cytotoxic and anticancer effects by enhancing the Nrf2/HO-1 pathway through antioxidant mechanisms in U-87 MG cells.

3309-

SIL,

Silymarin as a Natural Antioxidant: An Overview of the Current Evidence and Perspectives

Review,

NA,

*ROS↓, (1) Direct scavenging free radicals and chelating free Fe and Cu are mainly effective in the gut.
*IronCh↑,
*MMP↑, (2) Preventing free radical formation by inhibiting specific ROS-producing enzymes, or improving an integrity of mitochondria in stress conditions, are of great importance.
*NRF2↑, (3) Maintaining an optimal redox balance in the cell by activating a range of antioxidant enzymes and non-enzymatic antioxidants, mainly via Nrf2 activation
*Inflam↓, (4) Decreasing inflammatory responses by inhibiting NF-κB pathways is an emerging mechanism of SM protective effects in liver toxicity and various liver diseases.
*hepatoP↑,
*HSPs↑, (5) Activating vitagenes, responsible for synthesis of protective molecules, including heat shock proteins (HSPs), thioredoxin and sirtuins
*Trx↑,
*SIRT2↑, increased expression of protective molecules (GSH, Thioredoxins, heat shock proteins (HSPs), sirtuins, etc.)
*GSH↑,
*ROS↑, Similarly, production of O2− and NO in isolated rat Kupffer cells were inhibited by silibinin in a dose-dependent manner, with IC50 80 μM
*NADPH↓, It also decreased the NADPH oxidase, iNOS and NF-κB over expression by As and upregulated the Nrf2 expression in the renal tissue.
*iNOS↓,
*NF-kB↓,
*BioAv↓, active free silibinin concentration in plasma after oral consumption of SM, depending on dose of supplementation, could be in the range 0.2–2.0 μM.
*Dose↝, healthy volunteers, after an oral administration of SM (equivalent to 120 mg silibinin), total (unconjugated + conjugated) silibinin concentration in plasma was 1.1–1.3 μg/mL
*BioAv↑, For example, silibinin concentration in the gut could reach 800 μM

4733-

SSE,

Selenium supplementation of lung epithelial cells enhances nuclear factor E2-related factor 2 (Nrf2) activation following thioredoxin reductase inhibition

NA,

Nor,

*selenoP↑, Se is required for the synthesis and function of selenoenzymes including thioredoxin (Trx) reductase-1 (TXNRD1) and glutathione peroxidases (GPx).
*Trx↑,
*GPx↑, TXNRD1 and GPX2 protein expression and enzymatic activity were significantly greater upon Se supplementation
*NRF2↑, Se levels positively influence Nrf2 activation and selenoenzyme responses following TXNRD1 inhibition.

3960-

Taur,

Versatile Triad Alliance: Bile Acid, Taurine and Microbiota

Review,

AD,

Review,

Stroke,

*ROS↓, prevention of oxidative stress, and inflammation.
*Inflam↓,
*GABA↑, It serves as an agonist of GABAA receptors and, through them, exerts its neuronal inhibitory, anxiolytic, and calming effect
*memory↑, Consequently, taurine promotes emotional learning ability, memory, and cognitive performance
*cognitive↑,
*iNOS↓, It reduces inducible nitric oxide synthase (iNOS), C-reactive protein (CRP),
*CRP↓,
*HO-1↑, In parallel, it increases the expressions of cytoprotective antioxidant proteins, such as heme oxygenase 1 (HO-1), peroxiredoxin (PRX), and thioredoxin (TRX), in macrophages [74].
*Prx↑,
*Trx↑,
*NRF2↑, inhibits reactive oxygen species by Kelch-like ECH-associated protein 1 (Keap-1)/nuclear factor erythroid-2-related factor (Nrf2)/heme oxygenase-1 (HO-1) pathway
*GSH↑, enhanced liver antioxidant capacities via glutathione (GSH), Trolox equivalent antioxidant capacity (TEAC), superoxide dismutase (SOD), and catalase (CAT), decreased lipid peroxidation and malondialdehyde (MDA) levels [
*SOD↑,
*Catalase↑,
*lipid-P↓,
*MDA↓,
*eff↝, Similar to free taurine [62,63,64], TUDCA has proven neuroprotective properties which were researched in the models of Alzheimer’s disease (AD)
*GutMicro↑, taurine has been associated with inhibited growth of harmful bacteria, including Proteobacteria and especially Helicobacter, and also increasing the production of SCFA in mouse feces [351] as well as the metabolism of taurine by microbiota
other↑, Similarly, taurine plays a protective role in acute ischemic stroke

Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 2, Catalase↑, 3, GPx↑, 3, GSH↑, 7, GSR↑, 2, GSS↑, 1, GSTs↑, 1, HO-1↑, 3, Keap1↓, 1, lipid-P↓, 3, MDA↓, 1, MDA↑, 1, NQO1↑, 3, NRF2↑, 7, NRF2⇅, 1, Prx↑, 2, ROS↓, 8, ROS↑, 1, selenoP↑, 1, SOD↑, 3, Trx↑, 10, TrxR↑, 1, TrxR1↑, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 2,

Mitochondria & Bioenergetics ⓘ

ATP↑, 2, MMP↑, 1, mtDam↓, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, GlucoseCon↓, 1, Glycolysis↝, 1, HK2↓, 1, lactateProd↓, 1, LDHA↓, 2, NADPH↓, 3, PFK2↓, 1, PKM2↓, 1, PPARγ↑, 1, PPP↓, 1, SIRT1↑, 1, SIRT2↑, 1,

Cell Death ⓘ

iNOS↓, 2, necrosis↓, 1,

Protein Folding & ER Stress ⓘ

HSP27↑, 1, HSPs↓, 1, HSPs↑, 2,

Proliferation, Differentiation & Cell State ⓘ

neuroG↑, 1,

Barriers & Transport ⓘ

BBB↑, 1, GLUT4↑, 1,

Immune & Inflammatory Signaling ⓘ

CRP↓, 1, IFN-γ↓, 1, IL1↓, 1, IL6↓, 1, Inflam↓, 6, NF-kB↓, 1, TNF-α↓, 2,

Synaptic & Neurotransmission ⓘ

BDNF↑, 1, GABA↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 2, Dose↝, 1, eff↑, 1, eff↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, CRP↓, 1, GutMicro↑, 2, IL6↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, AntiDiabetic↑, 1, cognitive↑, 1, hepatoP↑, 2, memory↑, 1, neuroP↑, 1, radioP↑, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 74

Scientific Paper Hit Count for: Trx, Thioredoxin

3 Silymarin (Milk Thistle) silibinin
1 Capsaicin
1 γ-linolenic acid (Borage Oil)
1 Honokiol
1 Radiotherapy/Radiation
1 Piperlongumine
1 Quercetin
1 Curcumin
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Selenite (Sodium)
1 Taurine

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#:824  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

Trx Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Drug Metabolism & Resistance ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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