miR‑497 inhibits proliferation and invasion in triple‑negative breast cancer cells via YAP1
- Yuan Li
- Kaiyao Hua
- Jiali Jin
- Lin Fang
Affiliations: Department of Breast and Thyroid Surgery, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu 213164, P.R. China, School of Medicine, Tongji University, Shanghai 200092, P.R. China, Department of Neurology, Kongjiang Hospital of Yangpu District, Shanghai 200093, P.R. China, Department of Breast and Thyroid Surgery, Shanghai No. 10 People's Hospital, Clinical College of Nanjing Medical University, Shanghai 200072, P.R. China
- Published online on: June 2, 2021 https://doi.org/10.3892/ol.2021.12841
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MicroRNA (miR)‑497 has been reported as a tumor suppressor in various cancer types. Nonetheless, the regulation of triple‑negative breast cancer (TNBC) by miR‑497 remains poorly understood. The present study aimed to investigate the potential function and mechanism of miR‑497 in TNBC. A total of 36 TNBC and matched non‑cancerous tissue samples were collected for analysis. Reverse transcription‑quantitative PCR was performed to detect the miR‑497 levels in TNBC tissue. The association between miR‑497 expression, clinical characteristics and survival was then analyzed. To investigate the role of miR‑497 in TNBC, MTT, colony formation, Transwell invasion, cell cycle and cell apoptosis assays were conducted following transfection of miR‑497 mimics into the MDA‑MB‑231 and MDA‑MB‑468 cell lines. Luciferase reporter assays and western blot analysis were used to confirm the regulation of a putative target of miR‑497. The results indicated that the expression of miR‑497 was downregulated in the TNBC specimens. Further analysis demonstrated that the expression of miR‑497 was downregulated in patients with advanced TNBC stages and that low miR‑497 was associated with poor prognosis in patients with TNBC. Transfection of miR‑497 mimics inhibited TNBC cell proliferation and increased cell apoptosis in MDA‑MB‑231 and MDA‑MB‑468 cells. Moreover, cell migration was inhibited following overexpression of miR‑497, which also led to the arrest of the breast cancer cells in the G0/G1 phase of the cell cycle. Yes‑associated protein 1 (YAP1), a critical molecule in the Hippo pathway, was identified as a target of miR‑497. Notably, the protein and mRNA expression levels of YAP1 in MDA‑MB‑231 and MDA‑MB‑468 cells were downregulated following overexpression of miR‑497. Overall, the findings of the present study indicated that miR‑497 inhibited TNBC cell proliferation and migration and induced cell apoptosis by negatively regulating YAP1 expression. Thus, targeting miR‑497 may represent a potential strategy for the treatment of TNBC.