Dysregulation of microRNA expression plays a pivotal role in the initiation and progression of a variety of human carcinomas including prostate cancer. Our previous studies have demonstrated that the silence of miR‐203 contributes to the invasiveness of malignant breast cancer cells by targeting SNAI2. However, the effects and underlying mechanisms of miR‐203/SNAI2 axis in prostate cancer have not been elucidated. The aim of this study is to explore the effects of miR‐203/SNAI2 axis on the biological characteristics of prostate carcinomas both in vitro and in vivo. We found that miR‐203 was significantly downregulated in prostate cancer cell lines compared with immortalized prostate epithelial cells using semi‐quantitative PCR and real‐time PCR, as well as in clinical prostate cancer tissues compared to normal tissues using TCGA analysis. Functionally, miR‐203 inhibited prostate cancer cell proliferation, migration, endothelial cell tube formation and cancer stemness in vitro. Meanwhile, overexpression of miR‐203 suppressed SNAI2 expression both in DU145 and PC3 cells. In addition, the in vivo study showed that miR‐203 suppressed tumorigenicity, metastasis and angiogenesis of DU145 cells. Ectopic expression of SNAI2 rescued the inhibitory effects of miR‐203 both in vitro and in vivo. Importantly, the EMT markers CDH1 and VIMENTIN were modulated by the miR‐203/SNAI2 axis. Furthermore, the GSK‐3β/β‐CATENIN signal pathway was suppressed by miR‐203 and could be reactivated by SNAI2. Taken together, this research unveiled the function of miR‐203/SNAI2 axis in tumorigenesis, angiogenesis, stemness, metastasis and GSK‐3β/β‐CATENIN signal pathway in prostate cancer and gave insights into miR‐203/SNAI2‐targeting therapy for prostate cancer patients. © 2018 IUBMB Life, 70(3):224–236, 2018
IUBMB Life – Wiley
Published: Jan 1, 2018
Keywords: ; ; ; ;
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