TCF3

Last update 08 May 2025

Basic Info

Synonyms

bHLHb21, Class B basic helix-loop-helix protein 21, E2A

+ [14]

Introduction

Transcriptional regulator involved in the initiation of neuronal differentiation and mesenchymal to epithelial transition (By similarity). Heterodimers between TCF3 and tissue-specific basic helix-loop-helix (bHLH) proteins play major roles in determining tissue-specific cell fate during embryogenesis, like muscle or early B-cell differentiation (By similarity). Together with TCF15, required for the mesenchymal to epithelial transition (By similarity). Dimers bind DNA on E-box motifs: 5'-CANNTG-3' (By similarity). Binds to the kappa-E2 site in the kappa immunoglobulin gene enhancer (PubMed:2493990). Binds to IEB1 and IEB2, which are short DNA sequences in the insulin gene transcription control region (By similarity). Facilitates ATOH7 binding to DNA at the consensus sequence 5'-CAGGTG-3', and positively regulates transcriptional activity.

100 Clinical Results associated with TCF3

100 Translational Medicine associated with TCF3

0 Patents (Medical) associated with TCF3

2,341

Literatures (Medical) associated with TCF3

01 Jul 2025·Journal of Hazardous Materials

Integrative transcriptomics analysis reveals convergent toxicological effects of perfluorooctanoic acid and perfluorooctane sulfonate on human liver: Evidence from multiple models

Article

Author: Yin, Nuoya ; Yang, Renjun ; Faiola, Francesco

Perfluorooctanoic acid and perfluorooctane sulfonate are well-known eight-carbon per- and polyfluoroalkyl substances (8C-PFAS) potentially toxic for the human liver. However, direct experimental evidence demonstrating their toxicity on the human liver remains limited. Consequently, this study aimed to extrapolate the 8C-PFAS liver toxicity mechanisms by leveraging omics data to integrate mouse and human findings. Through integration analyses of nine datasets (one human, six murine, and two rat), we identified 199 genes with known biological functions that are commonly affected by 8C-PFAS across species. We delineated a comprehensive regulatory network of 8C-PFAS toxicity, demonstrating that 8C-PFAS may trigger fatty liver disease by up-regulating CD36 and PPARα pathway; dysregulate xenobiotic metabolism by disrupting CAR and CYP family genes; and induce cancer by dysregulating WNT, TGFβ, FGF21, and P53 pathways. We also identified ATF3, EGR1, ESR1, NFATC4, SNAI2, TP53, and EZH2 as transcriptionally regulated by 8C-PFAS, along with PPARα, RXRα, FGFR1, TCF3, and SMAD3 as potentially functionally impacted. Collectively, these factors account for over 90 % of 8C-PFAS-affected key genes. This study not only developed a novel method for extrapolating human toxicity risks by integrating scattered toxicity evidence based on transcriptomics data, but also proposes new mechanisms by which 8C-PFAS contributes to fatty liver disease and cancer.

01 Jul 2025·Cellular Signalling

RORα inhibits proliferation and chemoresistance through AKR1A1-induced glucose and lipid reprogramming in gastric cancer

Article

Author: Chen, Mengding ; Wang, Zhengguang ; Wang, Xiaoshan ; Chen, Feixu ; Shen, Tong ; Wu, Yuwei

BACKGROUNDAbnormal glycolysis and lipid metabolism play important roles in the occurrence and development of gastric cancer (GC). Moreover, dysregulation of circadian genes is associated with metabolic reprogramming in the tumor microenvironment. This study aimed to determine the role of retinoic acid-related orphan receptor alpha (RORα) in glucose and lipid reprogramming in GC.METHODSThe effects on cell proliferation and chemoresistance in vitro and in vivo were studied using gain- and loss-of-function experiments. Glycolytic activity and lipid synthesis were assessed using a Seahorse assay and reagent kits. Moreover, the regulatory mechanisms were explored using half-life, coimmunoprecipitation (Co-IP), chromatin immunoprecipitation (ChIP), luciferase reporter and immunofluorescence colocalization assays in GC cells. In addition, the relationships of RORα with E47 and AKR1A1 were analyzed using public databases and retrospective clinicopathological analyses.RESULTSRORα deletion promoted cell proliferation and fluorouracil (5-FU) chemoresistance by increasing glycolytic activity and lipid synthesis. In contrast, SR1078, an RORα activator, reversed these changes and had a synergistic inhibitory effect on cell proliferation in combination with 2-deoxygulose glucose (2-DG) or atorvastatin. Mechanistically, aldo-keto reductase family 1 member A1 (AKR1A1), is the key driver of RORα-mediated glucose and lipid reprogramming. Specifically, E47 is an AKR1A1 transcription factor, and its stability is affected by β-catenin. RORα deletion indirectly promoted E47 protein stability through the up-regulation of β-catenin, leading to increased AKR1A1 transcriptional activity. Moreover, RORα, E47 and AKR1A1 expression was dysregulated, and associated with clinicopathological parameters and prognosis in patients with GC. These expression patterns including RORα-low, E47-high and AKR1A1-high expression patterns alone or in combination were correlated with reduced responsiveness, poor prognosis, increased standard uptake value (SUV) levels and lipid droplet formation.CONCLUSIONSThese findings reveal a novel mechanism by which RORα regulates glucose and lipid reprogramming and may be a promising target for GC treatment.

01 Apr 2025·HemaSphere

TP53 deletion as an MRD‐dependent risk factor in childhood B‐ALL: A post hoc analysis from a prospective cohort

Article

Author: Zhu, Xiaofan ; Yin, Zixi ; An, Wenbin ; Yang, Wenyu ; Wang, Ning ; Chen, Yumei ; Li, Jun ; Gao, Yangyang ; Zou, Yao ; Wang, Junxia ; Chen, Xia ; Chen, Xiaojuan ; Zhang, Li ; Guo, Ye

AbstractThe effect of TP53 alterations on childhood B‐cell acute lymphoblastic leukemia (B‐ALL) remains unclear. To investigate the prognostic value of TP53 deletion (TP53del) and TP53 mutation (TP53mut), this post hoc study used fluorescence in situ hybridization test to detect TP53del in 907 newly diagnosed B‐ALL patients from a prospective cohort of Chinese Children's Cancer Group ALL‐2015 trial. Targeted gene sequencing was used to identify TP53mut in 342 out of the 907 patients. TP53del was detected in 4.4% of patients. The frequency of hypodiploidy was higher in TP53del subgroup (7.5% vs. 0.5%, p = 0.002), but patients with TP53del were less likely to have other recurrent genetic abnormalities, including BCR::ABL1, ETV6::RUNX1, TCF3::PBX1 and KMT2A rearrangements. Univariable and multivariable analyses indicated that TP53del was an independent risk factor for overall survival (OS) and disease‐free survival (DFS). Furthermore, stratification analysis revealed that TP53del was associated with lower 5‐year DFS in patients with positive minimal residual disease (MRD) after induction in the intermediate‐risk group (0.0% vs. 58.0% [95% confidence interval [CI] 49.2%–68.3%], p < 0.001), suggesting an MRD‐dependent pattern. However, somatic TP53mut was not associated with poor survival (81.8% [95% CI 61.9%–100.0%] vs. 84.9% [95% CI 81.1%‐89.0%], p = 0.971). In summary, TP53del may serve as a predictor for poor prognosis in pediatric B‐ALL. In particular, children in the intermediate‐risk group with positive MRD and TP53del may require more aggressive treatment.

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TCF3

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