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击败AR促进骨质母细胞通过改变外体circ-DHPS/miR-214-3p/CCL5通路来招募前列腺癌细胞

Zhao Yang¹, Jia-Qi Chen, Tian-Jie Liu

¹Department of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.

Asian journal of andrology

|November 15, 2023

概括

前列腺癌细胞中的雄激素受体 (AR) 信号影响外体体载荷,促进骨转移. 阻止circ-DHPS/miR-214-3p/CCL5通路可能会抑制这种外体介导的细胞迁移.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

前列腺癌 (PCa) 骨转移是一个重大的临床挑战.
来自瘤的外体细胞介导器官特异性转移.
雄激素受体 (AR) 在外体介导的PCa骨转移中的作用仍然不清楚.

研究的目的:

为了研究AR是否调节PCa细胞通过外体通过骨微环境的招募.
阐明导致PCa细胞迁移到骨质母细胞的外体介导的分子机制.

主要方法:

前列腺癌细胞培养和外体隔离.
安德روج因受体 (AR) 敲击和恩扎胺治疗.
异构体的表征和跟踪.
循环RNA (circRNA) 和微RNA (miRNA) 表达式分析.
骨质细胞共同培养和细胞迁移试验.

主要成果:

来自AR沉默或受酶胺治疗的PCa细胞的外体细胞促进了PCa细胞迁移到骨质母细胞.
抗逆转基因抑制增加了PCa细胞中的circ-DHPS表达,这种表达是外体运输的.
环-DHPS作为miR-214-3p的ceRNA,在骨质母细胞中对CCL5进行上调.
骨质母细胞中CCL5升高增强了PCa细胞的招募.

结论:

AR信号影响PCa中的外体组合和功能.
环-DHPS/miR-214-3p/CCL5轴是外体驱动PCa细胞迁移到骨的关键媒介.
针对这种途径可能提供一种治疗策略,以抑制PCa骨转移.

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