期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 435, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2021.115850
关键词
Cigarette smoke; Epithelial-mesenchymal transition; Prostate; Exosomes; Circ_0001359; Collagen deposition
资金
- State Natural Sciences Fund of China [81703594]
- High:level Talent Scientific Research Fund of Jianghan University [1010/08490001]
Cigarette smoke exposure promotes prostatic fibrosis. Circ_0001359 derived from CS-WPMY-1-exo contributes to prostatic fibrosis by stimulating epithelial cells phenotypes changes and collagen deposition.
Cigarettes consumption is continued to be popular. We found that cigarette smoke (CS) exposure promoted prostatic fibrosis. In this study, human prostate epithelial RWPE-1 cells were co-cultured with exosomes derived from CS exposed-WPMY-1 cells (CS-WPMY-1-exo). The collagen deposition, primary ciliogenesis, epithelialmesenchymal transition (EMT) and transforming growth factor (TGF)-beta 1 level of RWPE-1 were evaluated. The circRNAs profiles of WPMY-1-exo were explored by high-throughput RNA sequencing. It was found that CSWPMY-1-exo significantly promoted RWPE-1 collagen deposition, EMT and primary ciliogenesis. There were 17 differentially expressed (DE) circRNAs (including circ_0001359) between CS-WPMY-1-exo and the negative control. Functional enrichment analyses showed that the DE circRNAs played important roles in ciliary basal body, spindle microtubule and TGF-beta signaling pathway. Circ_0001359 siRNA attenuated CS-WPMY-1 induced RWPE-1 cells collagen deposition, EMT and primary ciliogenesis, as well as inhibited the level of TGF-beta 1. The whole results showed that circ_0001359 derived from CS-WPMY-1-exo contributed to prostatic fibrosis via stimulating epithelial cells phenotypes changes and collagen deposition.
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