TXNIP Cancer Research Results

TXNIP, TBP-2: Click to Expand ⟱
Source:
Type:
TXNIP {TBP-2 (Thioredoxin Binding Protein-2)} is broadly considered a tumor suppressor, given its roles in redox regulation, apoptosis, and cellular metabolism.
- Thioredoxin‐interacting protein (TXNIP), which belongs to the arrestin family and is induced by various stimuli, interacts with and inhibits thioredoxin activity.

- Lower TXNIP expression has been correlated with more aggressive disease features and poorer prognosis, while higher expression tends to associate with less aggressive phenotypes.
- A consistent theme across these cancers is that lower TXNIP expression frequently correlates with more aggressive disease and a worse prognosis.
Scientific Papers found: Click to Expand⟱
2637- Api,    Apigenin Alleviates Endoplasmic Reticulum Stress-Mediated Apoptosis in INS-1 β-Cells
- in-vitro, Diabetic, NA
*other↝, In the present study, the anti-diabetic effect of apigenin on pancreatic β-cell insulin secretion, apoptosis, and the mechanism underlying its anti-diabetic effects, were investigated in the INS-ID β-cell line
*Insulin↑, The results showed that apigenin concentration-dependently facilitated 11.1-mM glucose-induced insulin secretion, which peaked at 30 µM
ER Stress↓, Apigenin also concentration-dependently inhibited the expression of endoplasmic reticulum (ER) stress signaling proteins
*CHOP↓, CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) and cleaved caspase-3
*cl‑Casp3↓,
*ROS↓, In contrast, the cytoprotective effect of apigenin against oxidative stress, inflammation, apoptosis, and oxidative and ER stresses has been demonstrated in various cell types
*Inflam↓,
*TXNIP↓, expression of TXNIP, which was increased by the thapsigargin treatment, was downregulated in INS-1D cells in response to apigenin.

3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.

3225- EGCG,    Epigallocatechin‐3‐Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL‐1β Signaling Pathway
- in-vitro, Nor, NA - in-vivo, Nor, NA
*RenoP↑, EGCG improved kidney function, reduced albuminuria and body weight, and alleviated renal pathological damage.
*NLRP3↓, EGCG treatment reduced the expression of the NLRP3 inflammasome and its associated proteins, including TXNIP, ASC, caspase‐1, and IL‐1β, as well as the levels of ROS and inflammatory factors such as TNF‐α, IL‐6, and IL‐18.
*TXNIP↓,
*ASC↓,
*Casp1↓,
*IL1β↓,
*ROS↓,
*TNF-α↓,
*IL6↓,
*IL18↓,

2921- LT,    Luteolin as a potential hepatoprotective drug: Molecular mechanisms and treatment strategies
- Review, Nor, NA
*hepatoP↑, Due to its excellent liver protective effect, luteolin is an attractive molecule for the development of highly promising liver protective drugs.
*AMPK↑, fig2
*SIRT1↑,
*ROS↓,
STAT3↓,
TNF-α↓,
NF-kB↓,
*IL2↓,
*IFN-γ↓,
*GSH↑,
*SREBP1↓,
*ZO-1↑,
*TLR4↓,
BAX↑, anti cancer
Bcl-2↓,
XIAP↓,
Fas↑,
Casp8↑,
Beclin-1↑,
*TXNIP↓, luteolin inhibited TXNIP, caspase-1, interleukin-1β (IL-1β) and IL-18 to prevent the activation of NLRP3 inflammasome, thereby alleviating liver injury.
*Casp1↓,
*IL1β↓,
*IL18↓,
*NLRP3↓,
*MDA↓, inhibiting oxidative stress and regulating the level of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH)
*SOD↑,
*NRF2↑, luteolin promoted the activation of the Nrf2/ antioxidant response element (ARE) pathway and NF-κB cell apoptosis pathway, thereby reversing the decrease in Nrf2 levels(lead induced liver injury)
*ER Stress↓, down regulate the formation of nitrotyrosine (NT) and endoplasmic reticulum (ER) stress induced by acetaminophen, and alleviate liver injury
*ALAT↓, ↓ALT, AST, MDA, iNOS, NLRP3 ↑GSH, SOD, Nrf2
*AST↓,
*iNOS↓,
*IL6↓, ↓TXNIP, NLRP3, TNF-α, IL-6 ↑HO-1, NQO1
*HO-1↑,
*NQO1↑,
*PPARα↑, ↓TNF-α, IL-6 IL-1β, Bax ↑PPARα
*ATF4↓, ↓ALT, AST, TNF-α, IL-6, MDA, ATF-4, CHOP ↑GSH, SOD
*CHOP↓,
*Inflam↓, Luteolin ameliorates MAFLD through anti-inflammatory and antioxidant effects
*antiOx↑,
*GutMicro↑, luteolin could significantly enrich more than 10% of intestinal bacterial species, thereby increasing the abundance of ZO-1, down regulating intestinal permeability and plasma lipopolysaccharide

2456- MET,    Direct inhibition of hexokinase activity by metformin at least partially impairs glucose metabolism and tumor growth in experimental breast cancer
- in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
GlucoseCon↓, 1 mM metformin treatment markedly reduced cancer glucose consumption and growth.
TumCG↓,
HK2↓, our results strongly suggest that HK inhibition contributes to metformin therapeutic and preventive potential in breast cancer.
p‑AMPK↑, The reduction in glycolytic rate throughout the whole 48 h experiment duration was paralleled by a progressive increase in AMPK phosphorylation and by a progressive reduction (Fig. 1B) in TXNIP gene expression
TXNIP↓,
*toxicity↓, The experiment was completed in all animals, and no side effects occurred at the drug dosage used. As shown in Table 1, body weight was not significantly different in the 3 groups of animals

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↓,

4297- QC,    Quercetin attenuates tau hyperphosphorylation and improves cognitive disorder via suppression of ER stress in a manner dependent on AMPK pathway
- in-vitro, AD, SH-SY5Y
*AMPK↑, administration of quercetin enhanced AMPK activity, inhibited IRE1α and PERK phosphorylation, NLRP3 expression and tau phosphorylation
*IRE1↓,
*p‑PERK↓,
*p‑tau↓,
*cognitive↑, and improved cognitive disorder in mice exposed to high fat diets
*antiOx↑, exert anti-oxidative, anti-ER stress, anti-inflammatory activities and regulating glucose homeostasis, which can prevent neurodegenerative disorders, diabetes, and obesity
*ER Stress↓,
*Inflam↓,
*neuroP↑,
*TXNIP↓, Quercetin and quercetin-3-O-glucuronide suppressed ER stress with decreased phosphorylation of IRE1α and PERK, thereby inhibited TXNIP and NLRP3 inflammasome activation,
*NLRP3↓, effectively protected neuronal cells from inflammatory insult by blocking ER stress/NLRP3 inflammasome activation.

2092- TQ,    Dissecting the Potential Roles of Nigella sativa and Its Constituent Thymoquinone on the Prevention and on the Progression of Alzheimer's Disease
- Review, AD, NA
*iNOS↓, PC12normal: downregulated the iNOS expression along with NO level; (5) had a protective role of intracellular oxidative stress, by restoring the ROS level
*ROS↓,
*GSH↑, SH-SY5Y(normal): increasing the GSH levels.
*neuroP↑, TQ was able to reduce the neurotoxicity induced by Aß in an in vitro model of undifferentiated pheochromocytoma rat cell line, PC-12,
*MMPs↓, reestablishment of the abnormal levels of Matrix metalloproteinases (MMPs) and ROS
*MMP↑, E18, through the inhibition of ROS formation, and mitochondrial membrane depolarization.
*TXNIP↓, TQ was able to downregulate ... Thioredoxin-interacting protein (Txnip) and to upregulate the expression of Peroxiredoxin 1 (Prdx 1)
*Prx↑,
*memory↑, Bargi et al. (2017), reported that TQ was able, yet at lower doses, to improve memory impairments induced by LPS in rats.
*MDA↓, decreased level of markers of oxidative damage in brain tissues such as NOS, malondialdehyde (MDA) as well as an increased activity of SOD and catalase in hippocampus and cortex
*SOD↑,
*Catalase↑,
*BioAv↑, nanoemulsion may enhance the oral bioavailability and brain delivery.


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

p‑AMPK↑, 1,   GlucoseCon↓, 1,   HK2↓, 1,  

Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Casp8↑, 1,   Fas↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,   TumCG↓, 1,  

Migration ⓘ

TXNIP↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,   TNF-α↓, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 3,   HO-1↑, 3,   lipid-P↓, 1,   MDA↓, 3,   MPO↓, 1,   NQO1↑, 2,   NRF2↑, 3,   Prx↑, 1,   ROS↓, 6,   SOD↑, 4,   Trx1↑, 1,  

Mitochondria & Bioenergetics ⓘ

Insulin↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 3,   LDL↓, 1,   NADPH↓, 1,   PPARα↑, 1,   SIRT1↑, 2,   SREBP1↓, 1,  

Cell Death ⓘ

Casp1↓, 2,   cl‑Casp3↓, 1,   iNOS↓, 2,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Protein Folding & ER Stress ⓘ

CHOP↓, 2,   ER Stress↓, 2,   IRE1↓, 1,   p‑PERK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   mTOR↓, 1,  

Migration ⓘ

CDK5↓, 1,   MMPs↓, 1,   TXNIP↓, 7,   ZO-1↑, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↓, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   COX2↓, 1,   IFN-γ↓, 1,   IL10↑, 1,   IL17↓, 1,   IL18↓, 2,   IL1β↓, 3,   IL2↓, 1,   IL23↓, 1,   IL6↓, 2,   Inflam↓, 5,   MCP1↓, 1,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   BDNF↑, 2,   p‑tau↓, 3,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↓, 4,  

Hormonal & Nuclear Receptors ⓘ

ER(estro)↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,  

Clinical Biomarkers ⓘ

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

Functional Outcomes ⓘ

AntiAge↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 2,   neuroP↑, 4,   OS↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 74

Scientific Paper Hit Count for: TXNIP, TBP-2
1 Apigenin (mainly Parsley)
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Luteolin
1 Metformin
1 Methylsulfonylmethane
1 Quercetin
1 Thymoquinone
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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