ArticleCell cycle (Georgetown, Tex.)2015
TAp73 transcriptionally represses BNIP3 expression.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Single-cell mitophagy signature-based artificial intelligence model enhances prediction of prognosis and immunotherapy response in non-small-cell lung cancer.Respiratory research · 2026Article
- Exploring the relationship between sarcopenia and 11 respiratory diseases: a comprehensive mendelian randomization analysis.Aging clinical and experimental research · 2024Article
- Tax1 banding protein 1 exacerbates heart failure in mice by activating ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis.Acta pharmacologica Sinica · 2022Article
- The multifaceted role of autophagy in cancer.The EMBO journal · 2022Review
- TAp73 represses NF-κB-mediated recruitment of tumor-associated macrophages in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A Ferroptosis-Related Prognostic Signature Based on Antitumor Immunity and Tumor Protein p53 Mutation Exploration for Guiding Treatment in Patients With Head and Neck Squamous Cell Carcinoma.Frontiers in genetics · 2021Article
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Context is everything: extrinsic signalling and gain-of-function p53 mutants.Cell death discovery · 2020Review
- Mitophagy in Cancer: A Tale of Adaptation.Cells · 2019Review
- Article
- Association between TAp73, p53 and VASH1 expression in lung adenocarcinoma.Oncology letters · 2018Article
- Integrin-β4 is a novel transcriptional target of TAp73.Cell cycle (Georgetown, Tex.) · 2018Article
- Article
- P53 functional abnormality in mesenchymal stem cells promotes osteosarcoma development.Cell death & disease · 2016Review
- Diallyl disulfide enhances carbon ion beams-induced apoptotic cell death in cervical cancer cells through regulating Tap73 /ΔNp73.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 4 countries.
Funding
Abstract
TAp73 is a tumor suppressor transcriptional factor, belonging to p53 family. Alteration of TAp73 in tumors might lead to reduced DNA damage response, cell cycle arrest and apoptosis. Carcinogen-induced TAp73(-/-) tumors display also increased angiogenesis, associated to hyperactivition of hypoxia inducible factor signaling. Here, we show that TAp73 suppresses BNIP3 expression, directly binding its gene promoter. BNIP3 is a hypoxia responsive protein, involved in a variety of cellular processes, such as autophagy, mitophagy, apoptosis and necrotic-like cell death. Therefore, through different cellular process altered expression of BNIP3 may differently contribute to cancer development and progression. We found a significant upregulation of BNIP3 in human lung cancer datasets, and we identified a direct association between BNIP3 expression and survival rate of lung cancer patients. Our data therefore provide a novel transcriptional target of TAp73, associated to its antagonistic role on HIF signaling in cancer, which might play a role in tumor suppression.
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Registered trials
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.