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雄激素受体对DLGAP5的转录调控抑制了三阴性乳腺癌中的p53信号传导并抑制CD8+T细胞浸润。

Transcriptional regulation of DLGAP5 by AR suppresses p53 signaling and inhibits CD8T cell infiltration in triple-negative breast cancer.

作者信息

Pan Qing, Ma Dachang, Xiao Yi, Ji Kun, Wu Jun

机构信息

Department of Galactophore, The First Hospital of Lanzhou University, Lanzhou 730000, PR China.

Department of Galactophore, The First Hospital of Lanzhou University, Lanzhou 730000, PR China.

出版信息

Transl Oncol. 2024 Nov;49:102081. doi: 10.1016/j.tranon.2024.102081. Epub 2024 Aug 24.

DOI:10.1016/j.tranon.2024.102081
PMID:39182361
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11387711/
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 CD8T cell infiltration. This study highlights the crucial roles of AR and DLGAP5 in TNBC growth and immune cell infiltration. Taken together, AR inhibits the p53 signaling pathway by promoting DLGAP5 expression, thereby impacting CD8T cell infiltration in TNBC.

摘要

三阴性乳腺癌（TNBC）是一种生物学机制尚不清楚的具有挑战性的亚型。最近，转录因子雄激素受体（AR）及其对DLGAP5基因的调控在TNBC发病机制中受到关注。在本研究中，我们发现AR高表达与TNBC细胞增殖和生长之间存在正相关。此外，我们证实DLGAP5是AR在TNBC组织中高表达的关键下游调节因子。敲低DLGAP5可显著抑制TNBC细胞增殖、迁移和侵袭。观察到AR直接与DLGAP5启动子结合，增强其转录活性并抑制p53信号通路的激活。体内实验进一步证实，AR或DLGAP5的下调抑制肿瘤生长并增强CD8T细胞浸润。本研究突出了AR和DLGAP5在TNBC生长和免疫细胞浸润中的关键作用。综上所述，AR通过促进DLGAP5表达抑制p53信号通路，从而影响TNBC中的CD8T细胞浸润。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f11/11387711/e003c2dd3dc9/gr8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f11/11387711/cf003a263696/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f11/11387711/af9829acd434/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f11/11387711/c0f1b6177b8b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f11/11387711/fc6467dbfc37/gr4.jpg
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