ArticleCell death & disease2015
Candidate tumor suppressor B-cell translocation gene 3 impedes neoplastic progression by suppression of AKT.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- BTG3 suppresses oral squamous cell carcinoma progression by inhibiting PI3K/AKT signaling and EMT.Scientific reports · 2026Article
- Targeting miRNAs in renal cell carcinoma: emerging therapeutic strategies.International journal of clinical oncology · 2025Review
- BTG3-dependent VCP/p97 nuclear translocation is required for efficient repair of UV-induced DNA lesions.Nucleic acids research · 2025Article
- A keratinocyte-adipocyte signaling loop is reprogrammed by loss of BTG3 to augment skin carcinogenesis.Cell death and differentiation · 2024Article
- Role of Non-Coding RNAs in Colorectal Cancer: Focus on Long Non-Coding RNAs.International journal of molecular sciences · 2022Review
- The clinicopathological significances and related signal pathways of BTG3 mRNA expression in cancers: A bioinformatics analysis.Frontiers in genetics · 2022Article
- A Review of Recent Research on the Role of MicroRNAs in Renal Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2021Review
- Loss of the tumor suppressor BTG3 drives a pro-angiogenic tumor microenvironment through HIF-1 activation.Cell death & disease · 2020Article
- The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: An in vitro and vivo study.Oncotarget · 2017Article
- MicroRNA-142-5p promotes cell growth and migration in renal cell carcinoma by targeting BTG3.American journal of translational research · 2017Article
- FANCI is a negative regulator of Akt activation.Cell cycle (Georgetown, Tex.) · 2016Article
- The roles of BTG3 expression in gastric cancer: a potential marker for carcinogenesis and a target molecule for gene therapy.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BTG3 (B-cell translocation gene 3) is a p53 target that also binds and inhibits E2F1. Although it connects two major growth-regulatory pathways functionally and is downregulated in human cancers, whether and how BTG3 acts as a tumor suppressor remain largely uncharacterized. Here we present evidence that BTG3 binds and suppresses AKT, a kinase frequently deregulated in cancers. BTG3 ablation results in increased AKT activity that phosphorylates and inhibits glycogen synthase kinase 3β. Consequently, we also observed elevated β-catenin/T-cell factor activity, upregulation of mesenchymal markers, and enhanced cell migration. Consistent with these findings, BTG3 overexpression suppressed tumor growth in mouse xenografts, and was associated with diminished AKT phosphorylation and reduced β-catenin in tissue specimens. Significantly, a short BTG3-derived peptide was identified, which recapitulates these effects in vitro and in cells. Thus, our study provides mechanistic insights into a previously unreported AKT inhibitory pathway downstream of p53. The identification of an AKT inhibitory peptide also unveils a new avenue for cancer therapeutics development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.