GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR‐driven transcriptional activation

Aberrant transcriptional activation of the androgen receptor (AR) is a predominant cause of prostate cancer (PCa), including both in the initial and androgen‐independent stages. Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR‐driven transcriptional activity in PCa prog...

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Published in:Journal of cellular and molecular medicine Vol. 28; no. 20; pp. e70186 - n/a
Main Authors: Yan, Guang, Zhu, Tianhang, Zhou, Jiawei, Li, Xia, Wen, Zonghua, Miuhuitijiang, Bahaerguli, Zhang, Zhiyong, Du, Yuejun, Li, Chengyao, Shi, Xiaojun, Tan, Wanlong
Format: Journal Article
Language:English
Published: England John Wiley & Sons, Inc 01-10-2024
John Wiley and Sons Inc
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Summary:Aberrant transcriptional activation of the androgen receptor (AR) is a predominant cause of prostate cancer (PCa), including both in the initial and androgen‐independent stages. Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR‐driven transcriptional activity in PCa progression. Utilizing local clinical data and TCGA data, we have established a robust association between GOLM1 and AR target genes, and further demonstrated that GOLM1 can enhance the expression of AR target genes. We discovered that GOLM1 interacts with PSMD1, a component of the 19S regulatory complex in the 26S proteasome, using mass spectrometry and Co‐IP analysis. It is well known that ubiquitin‐proteasome plays a vital role in AR expression and transcriptional regulation. Our findings demonstrate that GOLM1 enhances ubiquitin proteasome activity by binding to PSMD1, thereby facilitating AR‐driven transcriptional activity and PCa progression. These results indicate that GOLM1 and its associated proteins may become potential therapeutic targets for PCa characterized by dysregulated AR‐driven transcriptional activation.
Bibliography:Guang Yan, Tianhang Zhu, and Jiawei Zhou contributed equally to this work.
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ISSN:1582-1838
1582-4934
1582-4934
DOI:10.1111/jcmm.70186