Tan Xiaoyu, Piao Yongyi, Yao Jiaxi, Zheng Changjian, Zhou Yu, Jiang Qing
Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, No. 76, Linjiang Road, Yuzhong District, Chongqing, 400010, China.
Department of Urology, Chongqing University Central Hospital, No. 1, Jiankang Road, Yuzhong District, 400010, Chongqing, China.
Med Oncol. 2025 Jun 28;42(8):297. doi: 10.1007/s12032-025-02866-3.
Prostate cancer remains one of the most common and aggressive cancers worldwide, but the molecular mechanisms underlying its progression are not yet fully understood. The ACSM1 gene is intimately associated with the development of prostate cancer. Here we demonstrated that down-regulation of ACSM1 expression in LNCaP prostate cancer cells significantly inhibits cell proliferation and migration, while overexpression enhances these processes in normal cells. Interestingly, the subcellular localization shift of ACSM1 to cytoplasm coincides with its interaction with 15-PGDH. Overexpression of ACSM1 also decreases 15-PGDH levels, increasing PGE2 production and altering ECM-related factors. Overexpression of 15-PGDH reverses these effects, suppressing the proliferation and migration of LNCaP cells. With specific PGE2 receptor inhibitors, AH6809 significantly affects the proliferation and migration of LNCaP cells with high ACSM1 expression. Based on our results, it appears that ACSM1 regulates prostate cancer cell behavior via the 15-PGDH-mediated PGE2 signaling pathway and Extracellular Matrix (ECM) remodeling.
前列腺癌仍然是全球最常见且侵袭性最强的癌症之一,但其进展背后的分子机制尚未完全明确。ACSM1基因与前列腺癌的发生密切相关。在此我们证明,LNCaP前列腺癌细胞中ACSM1表达的下调显著抑制细胞增殖和迁移,而在正常细胞中过表达则增强这些过程。有趣的是,ACSM1向细胞质的亚细胞定位转移与其与15 - PGDH的相互作用相一致。ACSM1的过表达还降低了15 - PGDH水平,增加了PGE2的产生并改变了与细胞外基质(ECM)相关的因子。15 - PGDH的过表达逆转了这些效应,抑制了LNCaP细胞的增殖和迁移。使用特异性PGE2受体抑制剂AH6809可显著影响ACSM1高表达的LNCaP细胞的增殖和迁移。基于我们的结果,ACSM1似乎通过15 - PGDH介导的PGE2信号通路和细胞外基质(ECM)重塑来调节前列腺癌细胞行为。