TET1 Cancer Research Results

TET1, Ten-Eleven Translocation 1: Click to Expand ⟱

Source:

Type:

TET1 (Ten-Eleven Translocation 1) is a gene that plays a crucial role in DNA demethylation and epigenetic regulation.
-Responsible for cell apoptosis, migration, and invasion.
TET1 is a member of the TET family of enzymes, which convert 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC) in DNA. This process is essential for maintaining genome stability, regulating gene expression, and preventing tumorigenesis.
TET1 is often downregulated or mutated, leading to decreased 5-hmC levels and aberrant DNA methylation patterns. This can result in the silencing of tumor suppressor genes and the activation of oncogenes, contributing to cancer development and progression.
-Loss of 5hmC is strongly associated with advanced and higher grade ccRCC.

Scientific Papers found: Click to Expand⟱

5464-

AF,

Inhibition of Thioredoxin-Reductase by Auranofin as a Pro-Oxidant Anticancer Strategy for Glioblastoma: In Vitro and In Vivo Studies

vitro+vivo,

GBM,

TrxR↓, Gold derivatives are irreversible inhibitors of TrxR. Among them, auranofin (AF), a selective TrxR inhibitor, has proven its effectiveness as a drug for the treatment of rheumatoid arthritis
BioAv↓, further clinical application of AF could be challenging due to the low solubility and insufficient delivery to glioblastoma.
ROS↑, The inhibition of TrxR1, which leads to increased ROS levels, is currently recognized as the primary mechanism of AF cytotoxicity [106]. In vitro studies have also shown that AF inhibits other thioredoxin reductases, such as TrxR2 and TrxR3
eff↝, The literature indicates that not all cancer tumors exhibit the same level of TrxR expression, affecting their sensitivity to AF.
TET1?, AF was shown to inhibit TET1 in T-ALL models
BioAv↑, Encapsulating AF into nanoparticles or combining it with other pharmaceutical excipients can minimize its potential adverse effects, preserve its interaction with serum proteins, and result in greater stability.

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

ROS↑, 1, TrxR↓, 1,

Migration ⓘ

TET1?, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 1, eff↝, 1,
Total Targets: 6

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: TET1, Ten-Eleven Translocation 1

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