TXNIP Cancer Research Results

TXNIP, TBP-2: Click to Expand ⟱
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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⟱
5634- BCA,    Molecular Mechanisms of Biochanin A in AML Cells: Apoptosis Induction and Pathway-Specific Regulation in U937 and THP-1
- in-vitro, AML, U937 - in-vitro, AML, THP1
Apoptosis↑, Biochanin A induced dose-dependent apoptosis, as evidenced by caspase-7 activation and PARP1 cleavage.
Casp7↑,
PARP1↑,
Bcl-2↓, Biochanin A downregulated oncogenes such as RUNX1, BCL2, and MYC while upregulating CHOP (GADD153), CDKN1A (p21), and SQSTM1 (p62), contributing to apoptosis and cell cycle arrest across both cell lines.
Myc↓,
CHOP↑,
P21↑,
p62↑,
TumCCA↑,
TXNIP↑, In contrast, in U937 cells, Biochanin A upregulated TXNIP and downregulated CCND2, highlighting the involvement of oxidative stress and G1/S cell cycle arrest.
ROS↑,
*antiOx↑, Biochanin A exhibits a broad spectrum of biological activities, including antioxidant, anti-inflammatory, estrogenic, metabolic regulatory, neuroprotective, and anticancer effects [1].
*Inflam↓,
*neuroP↑,
AntiCan↑,
TumCP↓, The anticancer mechanisms of Biochanin A involve the inhibition of cell proliferation via the modulation of cyclins and cyclin-dependent kinases
angioG↓, inhibition of angiogenesis and metastasis through downregulation of VEGF and matrix metalloproteinases (MMPs), and activation of apoptosis
TumMeta↓,
VEGF↓,
MMPs↓,
tumCV↓, Biochanin A significantly inhibited cell viability at concentrations ≥100 μM in U937 cells and ≥50 μM in THP-1 cells
DNAdam↑, Biochanin A induces a DNA damage response
CHOP↑, In our study, we observed a significant induction of CHOP protein expression following treatment with Biochanin A at concentrations of 100 μM and 200 μM.
cMyc↓, Biochanin A inhibited c-Myc protein expression in U937 and THP-1 cells
BioAv↓, Biochanin A remains limited due to its poor aqueous solubility and rapid systemic clearance, which render the 100–200 μM concentrations used in this study difficult to achieve in vivo
Half-Life↓,
BioAv↑, PEG-NLC formulations have been shown to significantly increase the plasma half-life and bioavailability of flavonoids

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.

2056- PB,    Endoplasmic Reticulum Stress Induces ROS Production and Activates NLRP3 Inflammasome Via the PERK-CHOP Signaling Pathway in Dry Eye Disease
- in-vitro, Nor, HCE-2
*ROS↓, We found that 4-PBA reduces ROS production and NLRP3 inflammasome activation, along with a decline in IL-1β expression.
*NLRP3↓,
*IL1β↓,
*TXNIP↑, activation of the TXNIP/NLRP3-IL1β signaling pathway
*ER Stress↓, In multiple studies, 4-PBA was shown to effectively suppress ER stress

2039- PB,    TXNIP mediates the differential responses of A549 cells to sodium butyrate and sodium 4‐phenylbutyrate treatment
- in-vitro, Lung, A549 - in-vitro, Nor, HEK293
TXNIP↑, TXNIP was strongly induced by NaBu (30‐ to 40‐fold mRNA) but was only slightly induced by 4PBA (two to fivefold) in A549 cells.
Casp3↑, Additionally, A549 cells that were treated with these showed changes in glucose consumption, caspase 3/7 activation and histone modifications, as well as enhanced mitochondrial superoxide production
Casp7↑,
mt-ROS↑, as well as enhanced mitochondrial superoxide production. 4PBA induced a mitochondrial superoxide‐associated cell death, while NaBu did so mainly through a TXNIP‐mediated pathway
GlucoseCon↓, both NaBu and 4PBA can decrease the glucose consumption compared to the vehicle control
TumCP↓, both inhibitors can prevent A549 cell proliferation and induce cell death
TumCD↑,
IGF-2↑, NaBu and 4PBA induce insulin‐like growth factor 2 (somatomedin A) (IGF2) 31‐fold and 48‐fold (Fig. S1 and S2), respectively.
HDAC↓, As inhibitors of HDACs, NaBu and 4PBA are capable of changing histone modifications
ROS⇅, suggests that 4PBA‐induced ROS generation might be a cell type or concentration dependent

2961- PL,    Piperlongumine inhibits esophageal squamous cell carcinoma in vitro and in vivo by triggering NRF2/ROS/TXNIP/NLRP3-dependent pyroptosis
- in-vitro, ESCC, KYSE-30
Pyro↑, PL significantly suppressed malignant behavior by promoting pyroptosis of ESCC cells by inhibiting proliferation, migration, invasion, and colony formation of KYSE-30 cells
TumCP↓,
TumCMig↓,
TumCI↓,
ASC↑, up-regulating expressions of ASC, Cleaved-caspase-1, NLRP3, and GSDMD, while inducing the generation of ROS.
cl‑Casp1↑,
NLRP3↑,
GSDMD↑,
ROS↑,
NRF2↓, PL inhibited the malignant behavior of ESCC cells in vitro and tumorigenesis of ESCC in vivo by inhibiting NRF2 and promoting ROS-TXNIP-NLRP3-mediated pyroptosis.
TXNIP↑,

2040- SAHA,    The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin
- in-vitro, Pca, LNCaP - in-vitro, CRC, T24/HTB-9 - in-vitro, BC, MCF-7
HDAC↓, SAHA) is a potent inhibitor of histone deacetylases (HDACs) that causes growth arrest, differentiation, and/or apoptosis of many tumor types in vitro and in vivo.
TumCG↓,
Diff↑,
Apoptosis↑,
TXNIP↑, SAHA induces the expression of vitamin D-up-regulated protein 1/thioredoxin-binding protein-2 (TBP-2) in transformed cells

2444- SFN,    Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage
- in-vitro, Nor, MRC-5
*GlucoseCon↓, SFN delayed senescence by decreasing glucose metabolism on the approach to senescence, exhibiting a caloric restriction mimetic-like activity
*ROS↓, and thereby decreased oxidative damage to cell protein and DNA
*Trx↓, This was associated with increased expression of thioredoxin-interacting protein, curbing entry of glucose into cells;
*HK2↓, decreased hexokinase-2
*NRF2↑, SFN is an activator of transcription factor Nrf2 [14] which regulates antioxidant response element- (ARE-) linked gene expression.
*Catalase↑, CAT, PDRX1, and GCLM, expression was increased in senescence and treatment with SFN increased the expression further
*TXNIP↑, increased expression of TXNIP, curbing the entry of glucose into cells
*PFKFB2↓, decreased PFKFB2 and increased G6PD, downregulating glycolysis.
*G6PD↑,


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↓, 1,   ROS↑, 3,   ROS⇅, 1,   mt-ROS↑, 1,   Trx1↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   GlucoseCon↓, 1,  

Cell Death ⓘ

Apoptosis↑, 3,   Bcl-2↓, 1,   cl‑Casp1↑, 1,   Casp3↑, 1,   Casp7↑, 2,   GSDMD↑, 1,   Myc↓, 1,   Pyro↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,  

Autophagy & Lysosomes ⓘ

p62↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   HDAC↓, 2,   IGF-2↑, 1,   TumCG↓, 2,  

Migration ⓘ

MMPs↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 3,   TumMeta↓, 1,   TXNIP↑, 5,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↑, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

Myc↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   NRF2↑, 1,   ROS↓, 2,   Trx↓, 1,  

Core Metabolism/Glycolysis ⓘ

G6PD↑, 1,   GlucoseCon↓, 1,   HK2↓, 1,   PFKFB2↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Migration ⓘ

TXNIP↑, 2,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Inflam↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,  
Total Targets: 15

Scientific Paper Hit Count for: TXNIP, TBP-2
2 Phenylbutyrate
1 Biochanin A
1 Curcumin
1 Resveratrol
1 Melatonin
1 Silymarin (Milk Thistle) silibinin
1 Piperlongumine
1 Vorinostat
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#:1237  State#:%  Dir#:2
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