ArticleTranslational oncology2024
Transcriptional regulation of DLGAP5 by AR suppresses p53 signaling and inhibits CD8
Article in Translational oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Androgens are a Key Factor Affecting Immune Related Diseases.The world journal of men's health · 2026Review
- Advances of androgen receptor in triple-negative breast cancer: from molecular mechanisms to clinical applications.Discover oncology · 2025Review
- Exercise-related immune gene signature for hepatocellular carcinoma: machine learning and multi-omics analysis.Frontiers in immunology · 2025Article
- The bioinformatics analysis and experimental validation of the carcinogenic role of EXO1 in lung adenocarcinoma.Frontiers in oncology · 2024Article
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Authors and funding
5 authors.
Funding
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Abstract
Triple-negative breast cancer (TNBC) is a challenging subtype with unclear biological mechanisms. Recently, the transcription factor androgen receptor (AR) and its regulation of the DLGAP5 gene have gained attention in TNBC pathogenesis. In this study, we found a positive correlation between high AR expression and TNBC cell proliferation and growth. Furthermore, we confirmed DLGAP5 as a critical downstream regulator of AR with high expression in TNBC tissues. Knockdown of DLGAP5 significantly inhibited TNBC cell proliferation, migration, and invasion. AR was observed to directly bind to the DLGAP5 promoter, enhancing its transcriptional activity and suppressing the activation of the p53 signaling pathway. In vivo experiments further validated that downregulation of AR or DLGAP5 inhibited tumor growth and enhanced CD8
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