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MicroRNA-132 通过 TGFβ1/Smad2 信号通路抑制人膀胱癌的迁移、侵袭和上皮 - 间质转化
Authors Wei XC, Lv ZH
Received 16 January 2019
Accepted for publication 25 March 2019
Published 23 July 2019 Volume 2019:12 Pages 5937—5945
DOI https://doi.org/10.2147/OTT.S201731
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Ms Rachel Predeepa
Peer reviewer comments 2
Editor who approved publication: Dr Federico Perche
Background and aim: Increasing evidence shows that microRNAs play an important regulatory role in the development of several types of cancers. However, the role of microRNA-132 (miR-132) in human bladder cancer (BC) metastasis remains unclear. In this research, we aimed to investigate the effect of miR-132 on the cell migration and relate potential mechanism in BC.
Methods: miR-132 expression level was assessed by quantitative real-time PCR (qRT-PCR) in 32 BC tissues and BC cell lines (T24). The function of miR-132 was evaluated by Transwell assay. Gene expression was determined by using qRT-PCR or Western blot.
Results: The results showed that miR-132 had a lower expression in BC tissues than in adjacent normal tissues. At the same time, compared to human normal urethral epithelium cells, the expression level of miR-132 was downregulated in T24 cell lines. miR-132 overexpression significantly inhibited migration and invasion capacities in T24 cells, while downregulation of miR-132 expression strengthened such capacities. Compared with those transfected with miR-132 mimic, EMT-related markers and TGFβ1/Smad2 expression levels were higher in T24 cells transfected with miR-132 inhibitor. Moreover, EMT-related markers and Smad2 expression levels was obviously increased in BC tissues compared to the adjacent normal tissues. The correlation result indicated that the expression of miR-132 and Smad2 was reversed.
Conclusion: In short, our results suggest that miR-132 may play a suppressive role in the metastasis of BC cells via TGFβ1/Smad2 signaling pathway.
Keywords: human bladder cancer, microRNA-132, metastasis, epithelial-mesenchymal transition