Trx1 Cancer Research Results

Trx1, Thioredoxin 1: Click to Expand ⟱
Source:
Type: serum marker BC
Trx1 is useful for the early diagnosis of breast cancer or the early prediction prognosis of breast cancer, and therefore has a valuable use as a diagnostic marker and companion marker to CEA and CA15-3 for breast cancer.
- Cytosolic thioredoxin (TRX-1) vs mitochondrial thioredoxin (TRX-2).
The Trx1 level of patients with other types of cancer was close to that of women without cancer, indicating that the blood Trx1 level has potential to could discern BC from other types of cancer.

Many tumor types, including lung, breast, colon, and prostate cancers, have shown elevated levels of TRX.
Scientific Papers found: Click to Expand⟱
4264- CA,    Carnosic Acid Mitigates Depression-Like Behavior in Ovariectomized Mice via Activation of Nrf2HO-1 Pathway
- in-vivo, NA, NA
*NRF2↑, CA treatment alleviated depressive behavior, induced the expression of Nrf2, HO-1, thioredoxin-1, and brain-derived neurotrophic factor, and enhanced serotonin levels.
*HO-1↑,
*Trx1↑,
*BDNF↑,
*5HT↑,
*ROS↓, CA also suppressed oxidative stress, reduced TNF-α, IL-1β, and iNOS mRNA expression, and ameliorated OVX-induced histopathological changes.
*TNF-α↓,
*IL1β↓,
*iNOS↓,

7180- CHA,    Chaetocin: A review of its anticancer potentials and mechanisms
- Review, Var, NA
TumCG↓, . Several studies have demonstrated that chaetocin suppresses the growth and proliferation of various tumour cells by regulating multiple signalling pathways related
TumCP↓,
Apoptosis↑, inducing cancer cell apoptosis (intrinsic and extrinsic), enhancing autophagy, inducing cell cycle arrest, and inhibiting tumour angiogenesis, invasion, and migration.
TumCCA↑,
angioG↓,
TumCI↓,
TumCMig↓,
SUV39H↓, chaetocin inhibits the activities of histone lysine methyltransferase SUV39H1
TrxR↓, formed covalent adducts with numerous proteins, including the thioredoxin-thioredoxin reductase (Trx-TrxR) system, hypoxia inducible factor-1 alpha (HIF-1α), heat shock protein 90 (Hsp90)
Hif1a↓,
HSP90↓,
ox-Trx1↑, ↑ oxidized TRX-1 & ROS activation; ↓ PI3K/AKT pathway & p-AKT; ↑ caspase-3, caspase-8 & caspase-9 activation; ↑ cleaved PARP proteins; ↓ BCL-2, BCL-XL, MCL-1, XIAP
ROS↑,
PI3K↓,
Akt↓,
Casp3↑,
Casp8↑,
Casp9↑,
cl‑PARP↑,
Bcl-2↓,
Bcl-xL↓,
Mcl-1↓,
XIAP↓,
DR5↑, ↑ DR5 & CHOP, ATF3;
CHOP/DDIT3↑,
ATF3↑,
angioG↓, chaetocin also indirectly targets tumour cells by inducing antiangiogenic effects in the tumour microvasculature.
VEGF↑, robust decrease in secreted VEGF in the culture media of treated cells and subsequent downregulation of the target genes of VEGFA, LDHA, ENO1 and HZF-1,
LDHA↓,
ENO1↓,

7185- CHA,    Chaetocin-induced ROS-mediated apoptosis involves ATM–YAP1 axis and JNK-dependent inhibition of glucose metabolism
- vitro+vivo, GBM, A172 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HMTs↓, Chaetocin, a histone methyltransferase inhibitor, is known to induce ROS generation.
ROS↑,
p‑ATM↑, Chaetocin-treated tumors exhibited heightened ROS, pATM, YAP1 and pJNK levels
YAP/TEAD↑, An increase in YAP1 level and decrease in YAP1 phosphorylation was observed upon Chaetocin treatment
p‑JNK↑,
TumPF↓, Chaetocin inhibits glioma cell proliferation
SUV39H↓, Chaetocin, an inhibitor of lysine-specific histone methyltransferase SUV39H1
TrxR↓, Chaetocin reduces thioredoxin reductase activity in a dose-dependent manner.
Casp3↑, Treatment with Chaetocin resulted in ∼3–5-fold increase in caspase-3 activity
Trx1↓, Chaetocin decreases the expression of TRX-1 in glioma cells
H3↓, Chaetocin-mediated inhibition of histone H3 methylation is ROS dependent
lactateProd↓, Chaetocin decreases lactate levels, ATP production and glucose uptake in a ROS- and JNK-dependent manner
ATP↓,
GlucoseCon↓,
TumCG↓, Chaetocin inhibits growth of tumor xenograft in nude mice
Dose↝, 10 animals each and were administered either with vehicle or Chaetocin (0.5 mg/kg body weight), intraperitoneally on alternate days for 25 days.

7167- CHA,    Chaetocin-induced ROS-mediated apoptosis involves ATM-YAP1 axis and JNK-dependent inhibition of glucose metabolism
- vitro+vivo, GBM, A172 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HMTs↓, Chaetocin, a histone methyltransferase inhibitor, is known to induce ROS generation.
ROS↑,
YAP/TEAD↑, Increased intracellular ROS induced (i) Yes-associated protein 1 (YAP1) expression independent of the canonical Hippo pathway as well as (ii) ATM and JNK activation.
ATM↑,
JNK↑,
Apoptosis↑, Increased interaction of YAP1 with p73 and p300 induced apoptosis in an ATM-dependent manner.
GlucoseCon↓, decreased ATP production was accompanied by a ROS/JNK-dependent decrease in cellular glucose uptake by glioma cells in the presence of Chaetocin
lactateProd↓, A significant decrease in lactate production (Figure 5d) and ATP generation (Figure 5e) was observed in Chaetocin-treated cells as compared with the untreated control.
ATP↓,
TumCP↓, Chaetocin inhibits glioma cell proliferation
TrxR↓, Chaetocin treatment reduced thioredoxin reductase activity in a dose-dependent manner with ∼40% decrease in activity observed at 1 μM concentration
Trx1↓, Chaetocin decreases the expression of TRX-1 in glioma cells
H3K9↓, The decrease in H3K9me3 levels observed upon Chaetocin treatment was reverted in the presence of ROS inhibitor NAc
p‑ATM↑, Chaetocin induced an increase in pATM and γH2AX expression in a ROS-dependent manner
γH2AX↑,
ALDOB↑, ALDOB, ENO3, FBP1, FBP2 G6PC, GCK GSK3B, GYS2, HK3, PCK1, PGK2, PGM3, PHKG1, PKLR, PRPS1L1 and PYGM) were elevated by more than 2 fold upon Chaetocin treatment
ENO3↑,
FBP1↑,
GSK‐3β↑,
HK3↑,
PCK1↑,
PGK2↑,
PGM1↑,
PGM3↑,
PHKG1↑,
PKLR↑, PKLR, up-regulated by 20.9
HK2↓, HK2, downregulated by 4.5 fold
PCNA↓, Decrease in both PCNA-positive cells and its protein level in Chaetocin-treated tumors indicated inhibition of cell proliferation

6225- CUR,    Natural products for enhancing the sensitivity or decreasing the adverse effects of anticancer drugs through regulating the redox balance
- Review, Var, NA
ox-Trx1↑, Curcumin increases Trx1 oxidation and subsequent apoptosis in prostate cancer cells [95].
TrxR1↓, (curcuminoid B63) has been shown to induce ROS-mediated paraptosis-like cell death by targeting TrxR1 in gastric cancer cells
TrxR↓, curcumin-induced inhibition of TrxR may depend on its Michael acceptor function.
ROS↑, leads to dramatic pro-oxidant effects, the induction of NOX activity, and the production of ROS
GSH/GSSG↓, significant decrease in the GSH/GSSG ratio was observed in lung cancer cells after treatment with curcumin
eff↓, NAC partially or completely reversed these effects, suggesting that ROS generation may be the underlying cause of curcumin-induced cell death.
Fenton↑, curcumin reduces Cu(II) to Cu(I) and leads to the formation of H2O2, which further reacts with Cu(I) through the Fenton reaction to produce •OH.
H2O2↑,
*NRF2↑, curcumin pretreatment significantly increases Nrf2 in the nucleus and decreases the expression of Keap1, as well as reverses the doxorubicin-induced reduction of HO-1 and NQO1, which provides a rational mechanism against doxorubicin-induced neurotoxi
*Keap1↓,
*HO-1↑,
*NQO1↑,
ChemoSen↑, The cisplatin and curcumin coloaded liposome system extends the drug duration and promotes drug accumulation in tumours.

1978- CUR,    Curcumin targeting the thioredoxin system elevates oxidative stress in HeLa cells
- in-vitro, Cerv, HeLa
TrxR1↓, curcumin can target the cytosolic/nuclear thioredoxin system to eventually elevate oxidative stress in HeLa cells
ROS↑,
DNA-PK↑, subsequently induces DNA oxidative damage
eff↑, curcumin-pretreated HeLa cells are more sensitive to oxidative stress
Trx↓, down-regulates Trx1 level and decreases Trx activity in HeLa cells
Trx1↓,

408- CUR,    Cytotoxic, chemosensitizing and radiosensitizing effects of curcumin based on thioredoxin system inhibition in breast cancer cells: 2D vs. 3D cell culture system
- in-vitro, BC, MCF7
Trx1↓,

134- CUR,  RES,  MEL,  SIL,    Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑,
ROS↑, curcumin and resveratrol promote ROS production and induce apoptosis in LNCaP and PC-3.
Trx1↓, Melatonin and silibinin did not change the basal redox state in LNCaP and these compounds even caused a further TRX1 reduction in PC-3 cells.
TumCG↓, Melatonin and silibinin inhibit cell growth while curcumin and resveratrol induce apoptosis in prostate cancer cell
eff↓, NAC prevents curcumin-induced apoptosis
TXNIP↑, Resveratrol decreases TRX1 by increasing TXNIP mRNA levels in PC-3 cells.

1974- EGCG,    Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes
- in-vitro, Nor, NA
*ROS↓, suppressed the increase in intracellular reactive oxygen species (ROS), nitric oxide (NO),
*NO↓,
*MMP↑, preincubation of the cells with EGCG increased mitochondrial membrane potential (MMP) and reduced calcium ion ([Ca2+]i) load.
*i-Ca+2↓, EGCC Increased Mitochondrial Membrane Potential and Decreased [Ca2+]i
*HO-1↑, expression of SOD, Heme oxygenase-1 (HO-1), Catalase (CAT), GSH-PX, nuclear factor erythroid 2-related factor 2 (Nrf2), and thioredoxin-1 (Trx-1).
*Catalase↑,
*NRF2↑,
*Trx1↑,
*antiOx↑, EGCC Increased Antioxidant Capacity
*SOD↑, EGCC Decreased ROS and Increased SOD Generation
*Apoptosis↓,

1976- EGCG,    Epigallocatechin-3-gallate exhibits anti-tumor effect by perturbing redox homeostasis, modulating the release of pro-inflammatory mediators and decreasing the invasiveness of glioblastoma cells
- in-vitro, GBM, U87MG
ROS↑, Polyphenol epigallocatechin-3-gallate (EGCG) induced apoptosis in glioma cells by elevating oxidative stress through increased reactive oxygen species (ROS) generation. Signs of apoptosis included altered mitochondrial membrane potential and elevated
MMP↓, altered mitochondrial membrane potential
Casp3↑, elevated expression of caspase-3 (5fold) and cytochrome c
Cyt‑c↑,
Trx1↓, The increase in ROS was concomitant with the decrease in expression of thioredoxin (TRX-1)
Ceru↓, and ceruloplasmin (CP)
IL6↓, EGCG downregulated the levels of pro-inflammatory cytokine interleukin (IL)-6 and chemokines IL-8, monocyte-chemoattractant protein (MCP)-1 and RANTES
IL8↓,
MCP1/CCL2↓,
RANTES?,
uPA↝, 40-50% decrease in uPa activity was observed in glioma cells upon treatment with 50 and 100 uM of EGCG
ROS↑, ROS production, a significant 1.7- and 2-fold (p<0.05) increase in ROS production was observed in cells treated with 50 and 100 uM EGCG respectively,

1973- GamB,    Gambogic acid deactivates cytosolic and mitochondrial thioredoxins by covalent binding to the functional domain
- in-vitro, Liver, SMMC-7721 cell
Apoptosis↑, selectively induces apoptosis in cancer cells, at least partially, by targeting the stress response to reactive oxygen species (ROS).
ROS↑,
Trx↓, deactivates TRX-1/2 proteins by covalent binding to the active cysteine residues in the functional domain via Michael addition reactions.
Trx1↓,
Trx2↓,
Mich↑, can react with small nucleophilic molecules, such as GSH and a cysteine-containing peptide, via a Michael addition reaction.

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

2916- LT,    Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies
- Review, Var, NA - Review, AD, NA - Review, Park, NA
proCasp9↓, , by inactivating proteins; such as procaspase‐9, CDC2 and cyclin B or upregulation of caspase‐9 and caspase‐3, cytochrome C, cyclin A, CDK2, and APAF‐1, in turn inducing cell cycle
CDC2↓,
CycB/CCNB1↓,
Casp9↑,
Casp3↑,
Cyt‑c↑,
cycA1/CCNA1↑,
CDK2↓, inhibit CDK2 activity
APAF1↑,
TumCCA↑,
P53↑, enhances phosphorylation of p53 and expression level of p53‐targeted downstream gene.
BAX↑, Increasing BAX protein expression; decreasing VEGF and Bcl‐2 expression it can initiate cell cycle arrest and apoptosis.
VEGF↓,
Bcl-2↓,
Apoptosis↑,
p‑Akt↓, reduce expression levels of p‐Akt, p‐EGFR, p‐Erk1/2, and p‐STAT3.
p‑EGFR↓,
p‑ERK↓,
p‑STAT3↓,
cardioP↑, Luteolin plays positive role against cardiovascular disorders by improving cardiac function
Catalase↓, It can reduce activity levels of catalase, superoxide dismutase, and GS4
SOD↓,
*BioAv↓, bioavailability of luteolin is very low. Due to the momentous first pass effect, only 4.10% was found to be available from dosage of 50 mg/kg intake of luteolin
*antiOx↑, luteolin classically exhibits antioxidant features
*ROS↓, The antioxidant potential of luteolin and its glycosides is mainly due to scavenging activity against reactive oxygen species (ROS) and nitrogen species
*NO↓,
*GSTs↑, Luteolin may also have a role in protection and enhancement of endogenous antioxidants such as glutathione‐S‐transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT)
*GSR↑,
*SOD↑,
*Catalase↑,
*lipid-P↓, Luteolin supplementation significantly suppressed the lipid peroxidation
PI3K↓, inhibits PI3K/Akt signaling pathway to induce apoptosis
Akt↓,
CDK2↓, inhibit CDK2 activity
BNIP3↑, upregulation of BNIP3 gene
hTERT/TERT↓, Suppress hTERT in MDA‐MB‐231 breast cancer cel
DR5↑, Boost DR5 expression
Beclin-1↑, Activate beclin 1
TNF-α↓, Block TNF‐α, NF‐κB, IL‐1, IL‐6,
NF-kB↓,
IL1↓,
IL6↓,
EMT↓, Suppress EMT essentially notable in cancer metastasis
FAK↓, Block EGFR‐signaling pathway and FAK activity
E-cadherin↑, increasing E‐cadherin expression by inhibiting mdm2
MDM2↓,
NOTCH↓, Inhibit NOTCH signaling
MAPK↑, Activate MAPK to inhibit tumor growt
Vim↓, downregulation of vimentin, N‐cadherin, Snail, and induction of E‐cadherin expressions
N-cadherin↓,
Snail↓,
MMP2↓, negatively regulated MMP2 and TWIST1
Twist↓,
MMP9↓, Inhibit matrix metalloproteinase‐9 expressions;
ROS↑, Induce apoptosis, reactive oxygen development, promotion of mitochondrial autophagy, loss of mitochondrial membrane potential
MMP↓,
*AChE↓, Reduce AchE activity to slow down inception of Alzheimer's disease‐like symptoms
*MMP↑, Reverse mitochondrial membrane potential dissipation
*Aβ↓, Inhibit Aβ25‐35
*neuroP↑, reduces neuronal apoptosis; inhibits Aβ generation
Trx1↑, luteolin against human bladder cancer cell line T24 was due to induction cell‐cycle arrest at G2/M, downregulation of p‐S6, suppression of cell survival, upregulation of p21 and TRX1, reduction in ROS levels.
ROS↓,
*NRF2↑, Luteolin reduced renal injury by inhibiting XO activity, modulating uric acid transporters, as well as activating Nrf2 HO‐1/NQO1 antioxidant pathways and renal SIRT1/6 cascade.
NRF2↓, Luteolin exerted anticancer effects in HT29 cells as it inhibits nuclear factor‐erythroid‐2‐related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway
*BBB↑, Luteolin can be used to treat brain cancer due to ability of this molecule to easily cross the blood–brain barrier
ChemoSen↑, In ovarian cancer cells, luteolin chemosensitizes the cells through repressing the epithelial‐mesenchymal transition markers
GutMicro↑, Luteolin was also observed to modulate gut microbiota which reduce the number of tumors in case of colorectal cancer by enhancing the number of health‐related microbiota and reduced the microbiota related to inflammation

3848- MSM,    Modulatory effect of methylsulfonylmethane against BPA/γ-radiation induced neurodegenerative alterations in rats: Influence of TREM-2/DAP-12/Syk pathway
- in-vitro, AD, NA
*ROS↓, MSM treatment improved histopathological insults and ameliorated level of oxidative stress, neuroinflammation and AD markers as well as modulated TREM-2/DAP-12/Syk pathway.
*Inflam↓,
*neuroP↑, The crucial role of MSM in the exerted neuroprotection is elicited via enhancing estrogen receptors signaling (ERα and ERβ), restoring Nrf-2/HO-1 signaling and promoting redoxins (Trx-1 and Grx-1)
*ER(estro)↑,
*NRF2↑,
*HO-1↑,
*Trx1↑,
*TXNIP↓, along with inhibiting TXNIP, reducing oxidative stress (MDA and NOx) and up-regulating anti- oxidant machinery (GSH, GPx, SOD and CAT), d
*MDA↓,
*NOX↓,
*GSH↑,
*GPx↑,
*SOD↑,
*Catalase↑,
*BDNF↑, retrieving BDNF level and suppressing AchE activity, reducing tau-phosphorylation and curbing NFTs formation, decreasing AB production.
*AChE↓,
*p‑tau↓,
*Aβ↓,

1942- PL,    Piperlongumine inhibits antioxidant enzymes, increases ROS levels, induces DNA damage and G2/M cell cycle arrest in breast cell lines
- in-vitro, BC, MCF7
ROS↑, PLN increased ROS levels and expression of the SOD1 antioxidant enzyme
SOD1↑,
Trx1↓, PLN inhibited the expression of the antioxidant enzymes catalase, TRx1, and PRx2.
Catalase↓,
PrxII↓,
ROS↑, ability of PLN to inhibit antioxidant enzyme expression was associated with the oxidative stress response
GADD45A↑, upregulated the levels of GADD45A mRNA and p21 protein.
P21↑,
DNAdam↑, In response to elevated ROS levels and DNA damage induction, the cells were arrested at the G2/M phase
TumCCA↑, arrested at the G2/M phase

635- VitC,  VitK3,    The combination of ascorbate and menadione causes cancer cell death by oxidative stress and replicative stress
- in-vitro, NA, NA
RNR↓, VC/VK3 inhibited RNR mainly by targeting its R2 subunit
GSH↓,
Trx1↓, increased highly oxidized Trx1 (oxidized (and generally less active) means effectively less)
GPx↓, VC/VK3 inhibited glutathione peroxidase activity and led to an elevated level of lipid peroxidation, which triggered apoptosis-inducing factor (AIF) mediated cell death pathway.
lipid-P↑,
AIF↑, which triggered apoptosis-inducing factor (AIF) mediated cell death pathway
ROS↑,


Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

ALDOB↑, 1,   ENO3↑, 1,   H3K9↓, 1,   HK3↑, 1,   PGK2↑, 1,   PGM3↑, 1,   PHKG1↑, 1,   PKLR↑, 1,   SUV39H↓, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

ATF3↑, 1,   Catalase↓, 2,   Ceru↓, 1,   Fenton↑, 1,   GPx↓, 1,   GSH↓, 1,   GSH/GSSG↓, 1,   H2O2↑, 1,   lipid-P↑, 1,   Mich↑, 1,   NRF2↓, 1,   PrxII↓, 1,   ROS↓, 1,   ROS↑, 13,   SOD↓, 1,   SOD1↑, 1,   Trx↓, 2,   Trx1↓, 9,   Trx1↑, 1,   ox-Trx1↑, 2,   Trx2↓, 1,   TrxR↓, 4,   TrxR1↓, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   ATP↓, 2,   CDC2↓, 1,   MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ENO1↓, 1,   FBP1↑, 1,   GlucoseCon↓, 2,   HK2↓, 1,   lactateProd↓, 2,   LDHA↓, 1,   PCK1↑, 1,   PGM1↑, 1,   RNR↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 5,   BAX↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp3↑, 4,   Casp8↑, 1,   Casp9↑, 2,   proCasp9↓, 1,   Cyt‑c↑, 2,   DR5↑, 2,   hTERT/TERT↓, 1,   JNK↑, 1,   p‑JNK↑, 1,   MAPK↑, 1,   Mcl-1↓, 1,   MDM2↓, 1,   YAP/TEAD↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

H3↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   HSP90↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   BNIP3↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   p‑ATM↑, 2,   DNA-PK↑, 1,   DNAdam↑, 1,   GADD45A↑, 1,   P53↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   p‑ERK↓, 1,   GSK‐3β↑, 1,   HMTs↓, 2,   NOTCH↓, 1,   PI3K↓, 2,   p‑STAT3↓, 1,   TumCG↓, 3,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   FAK↓, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   Snail↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumPF↓, 1,   Twist↓, 1,   TXNIP↑, 1,   uPA↝, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   p‑EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1↓, 1,   IL6↓, 2,   IL8↓, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 1,   RANTES?, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

p‑EGFR↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,  
Total Targets: 129

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 3,   GPx↑, 1,   GSH↑, 2,   GSR↑, 1,   GSTs↑, 1,   HO-1↑, 5,   Keap1↓, 1,   lipid-P↓, 1,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 6,   ROS↓, 5,   SOD↑, 3,   Trx1↑, 4,   TrxR1↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

NADPH↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   iNOS↓, 1,  

Migration(tgid=13) ⓘ

i-Ca+2↓, 1,   TXNIP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 2,   BDNF↑, 2,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ER(estro)↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 3,  
Total Targets: 36

Scientific Paper Hit Count for: Trx1, Thioredoxin 1
4 Curcumin
3 chaetocin
2 EGCG (Epigallocatechin Gallate)
1 Carnosic acid
1 Resveratrol
1 Melatonin
1 Silymarin (Milk Thistle) silibinin
1 Gambogic Acid
1 Honokiol
1 Luteolin
1 Methylsulfonylmethane
1 Piperlongumine
1 Vitamin C (Ascorbic Acid)
1 VitK3,menadione
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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  wNotes=on  sortOrder:rid,rpid

 

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