Knocking down AR promotes osteoblasts to recruit prostate cancer cells by altering exosomal circ-DHPS/miR-214-3p/CCL5 pathway  

作　　者：Zhao Yang Jia-Qi Chen Tian-Jie Liu Yu-Le Chen Zhen-Kun Ma Yi-Zeng Fan Zi-Xi Wang Shan Xu Ke Wang Xin-Yang Wang Lei Li Hong-Jun Xie 

机构地区：[1]Department of Urology,The First Affiliated Hospital of Xi'an Jiaotong University,Xi'an 710061,China

出　　处：《Asian Journal of Andrology》2024年第2期195-204,共10页亚洲男性学杂志（英文版）

基　　金：supported by grant from the National Natural Science Foundation of China(No.82002693 and No.81803022);the Natural Science Foundation of Shaanxi Province(No.2022JQ-903 and No.2020JQ-519).

摘　　要：Tumor-derived exosomes have been shown to play a key role in organ-specific metastasis,and the androgen receptor regulates prostate cancer(PCa)progression.It is unclear whether the androgen receptor regulates the recruitment of prostate cancer cells to the bone microenvironment,even bone metastases,through exosomes.Here,we found that exosomes isolated from PCa cells after knocking down androgen receptor(AR)or enzalutamide treatment can facilitate the migration of prostate cancer cells to osteoblasts.In addition,AR silencing or treatment with the AR antagonist enzalutamide may increase the expression of circular RNA-deoxyhypusine synthase(circ-DHPS)in PCa cells,which can be transported to osteoblasts by exosomes.Circ-DHPS acts as a competitive endogenous RNA(ceRNA)against endogenous miR-214-3p to promote C-C chemokine ligand 5(CCL5)levels in osteoblasts.Increasing the level of CCL5 in osteoblasts could recruit more PCa cells into the bone microenvironment.Thus,blocking the circ-DHPS/miR-214-3p/CCL5 signal may decrease exosome-mediated migration of prostate cancer cells to osteoblasts.

关 键 词：androgen receptor circRNA EXOSOME prostate cancer 

分 类 号：R737.25[医药卫生—肿瘤]