期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 120, 期 9, 页码 15924-15932出版社
WILEY
DOI: 10.1002/jcb.28866
关键词
bladder cancer; migration; miR-30e-5p; metadherin; proliferation
资金
- National Natural Science Foundation of China [81772710, 81502203]
Recent studies have suggested that miR-30e-5p is dysregulated in several human carcinomas; however, the mechanism of miR-30e-5p in bladder cancer (BCa) remains unknown. Here, we confirmed that the expression of miR-30e-5p was decreased in human BCa specimens and cell lines by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Upregulation of miR-30e-5p decreased the proliferation and migration in T24 and UM-UC-3 cells. Metadherin (MTDH) was a potential target for miR-30e-5p through bioinformatics analysis. Dual-luciferase assays were conducted to validate the interaction between miR-30e-5p and MTDH, which demonstrates that the relative luciferase activity was significantly downregulated after transfected miR-30e-5p mimic compared with control mimic in 293T cells. We also detected that whether silencing of MTDH by using small interfering(si)-MTDH matched effects caused by miR-30e-5p overexpression in BCa cells lines by Cell Counting Kit-8 (CCK-8), colony formation, and transwell assay, and we found the effects of silencing of MTDH same as miR-30e-5p overexpression. Furthermore, we verified that the restoration of MTDH in miR-30e-5p-overexpressed BCa cells rescued the inhibitory effects of miR-30e-5p. In conclusion, these results demonstrated that miR-30e-5p may inhibit BCa cells growth and invasiveness by targeting MTDH and may be a promising therapeutic agent for treating clinical BCa patients.
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