Research Papers:

Enhancing E-cadherin expression via promoter-targeted miR-373 suppresses bladder cancer cells growth and metastasis

Qingsong Zhang, Chenghe Wang, Shuo Miao, Chuanchang Li, Zhong Chen _ and Fan Li

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Oncotarget. 2017; 8:93969-93983. https://doi.org/10.18632/oncotarget.21400

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Qingsong Zhang1,*, Chenghe Wang2,*, Shuo Miao3, Chuanchang Li1, Zhong Chen1 and Fan Li1

1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China

2Department of Urology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China

3Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China

*Qingsong Zhang and Chenghe Wang: Co-first author

Correspondence to:

Zhong Chen, email: [email protected]

Keywords: RNA activation, MiR-373, bladder cancer, proliferation, metastasis

Received: March 21, 2017    Accepted: September 18, 2017    Published: September 30, 2017


Previous studies showed that miR-373 had the capacity to induce tumor suppressor gene E-cadherin expression in prostate cancer cells. However, whether miR-373 can activate the expression of E-cadherin in human bladder cancer (BCa) cells and inhibit cells remains to be elucidated. Here, we found that both miR-373 and E-cadherin were low expressed in BCa tissues and cell lines, and significantly correlated with tumor stage, grade, and lymph node metastasis. In addition, decreased E-cadherin expression or low expression of both miR-373 and E-cadherin is associated with poor overall survival in patients with BCa. Transfection of miR-373 into BCa cells readily activated E-cadherin expression by targeting promoter. Moreover, miR-373 exhibited robust capacity to inhibit cells proliferation, suppress migration and invasion by enhancing E-cadherin expression, and significantly suppress the growth of xenografts and metastasis in nude mice. Altogether, our findings indicate that miR-373 may as a tumor suppressor in BCa by activating E-cadherin expression.

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