Cancer Cell International (Feb 2019)

miR-182-5p affects human bladder cancer cell proliferation, migration and invasion through regulating Cofilin 1

  • Fei Wang,
  • Dinglan Wu,
  • Zhanping Xu,
  • Jianxiang Chen,
  • Jiye Zhang,
  • Xiaojuan Li,
  • Shiliang Chen,
  • Fengrong He,
  • Jianbing Xu,
  • Liangju Su,
  • Defan Luo,
  • Shufang Zhang,
  • Weifu Wang

DOI
https://doi.org/10.1186/s12935-019-0758-5
Journal volume & issue
Vol. 19, no. 1
pp. 1 – 10

Abstract

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Abstract Background Human bladder cancer is one of the common malignant tumors, and it mainly occurs in men. miR-182-5p, a member of miR-183 family, acts as tumor suppressor or oncogene in various kinds of tumors. In this study, we first investigate that the absence of miR-182-5p in human bladder cancer promotes tumor growth by regulating the expression of Cofilin 1, an actin modulating-protein. Methods Human bladder tumor tissue specimens were collected to detect the expression of miR-182-5p and Cofilin 1 by qRT-PCR. Luciferase activity assay was performed to demonstrate the regulation of Cofilin 1 mRNA 3′UTR by miR-182-5p. Then, cell experiments were performed to analysis the effect of miR-182-5p/Cofilin 1 pathway on tumor cell proliferation, migration, invasion and colony forming efficiency. Finally, xenograft tumor models were established to evaluate the role of miR-182-5p in tumorigenesis abilities in vivo. Results qRT-PCR and Western blotting analysis showed that Cofilin 1 expression was up-regulated in both bladder cancer tissues and cell lines compared with normal. Luciferase activity assay showed that miR-182-5p specifically targets Cofilin 1 mRNA 3′UTR and represses the expression of Cofilin 1. Also, miR-182-5p inhibited bladder tumor cell proliferation, migration, invasion and colony forming efficiency. Furthermore, xenograft tumor model assay showed that miR-182-5p plays a negative role in bladder cancer tumorigenesis abilities in vivo. Conclusion Present results suggest that miR-182-5p could inhibit human bladder tumor growth by repressing Cofilin 1 expression. Our findings may provide a new horizon for exploring therapeutic target of bladder cancer.

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