MicroRNA‑192 inhibits cell proliferation and induces apoptosis in human breast cancer by targeting caveolin 1

• Published in: Oncology reports Vol. 42; no. 5; pp. 1667 - 1676
• Main Authors: Chen, Pinjia, Feng, Yun, Zhang, Haige, Shi, Xinpeng, Li, Bin, Ju, Wencui, Yu, Xiurong, Zhang, Nan, Luo, Xiaoyong
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.11.2019; D.A. Spandidos
• Subjects: 3' Untranslated Regions; Aged; Animals; Apoptosis; Breast cancer; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Caveolin 1 - genetics; Caveolin 1 - metabolism; Cell cycle; Cell growth; Cell Line, Tumor; Cell Proliferation; Down-Regulation; Drug resistance; Female; Gene expression; Gene Expression Regulation, Neoplastic; Humans; Liver cancer; MCF-7 Cells; Metastasis; Mice; MicroRNAs; MicroRNAs - genetics; Middle Aged; Neoplasm Transplantation; Prostate cancer; Protein expression; Proteins; Roles; Studies; United States > US; China
• ISSN: 1021-335X; 1791-2431
• DOI: 10.3892/or.2019.7298

It has been demonstrated that microRNA‑192 (miR‑192) serves important roles in different cancer types, including breast cancer, prostate cancer and colorectal cancer. However, its biological role and function in breast cancer remains largely unknown. The present study aimed to determine the role of miR‑192 in breast cancer. In the present study, one normal breast and two breast tumor cells lines were used, which included the normal mammary fibroblast cell line Hs578Bst, a more aggressive breast tumor cell line MDA‑MB‑231 and a less aggressive breast tumor cell line MCF‑7. The effect of miR‑192 on proliferation of breast cancer cells was detected with an MTT assay. Western blot analysis was performed to determine protein expression of caveolin 1 (CAV1). A lentiviral vector that overexpresses pre‑miR‑192 and control lentiviral packaging plasmids were used in the present study. The Student's t‑test was performed to analyze the significance of differences between samples. In the present study, it was determined that the expression of miR‑192 is downregulated in breast cancer, compared with the adjacent normal tissues. Overexpression of miR‑192 significantly inhibited cell proliferation, and induced cell apoptosis and cell cycle arrest in MCF7 and MDA‑MB‑231 cells. Using a bioinformatics method, CAV1 was considered a potential target of miR‑192. Furthermore, it was demonstrated that CAV1 is a direct target of miR‑192 and its protein expression is negatively regulated by miR‑192. Therefore, the present study demonstrated that miR‑192 serves an important role as a regulator in breast cancer and the miR‑192/CAV1 axis has a potential as a therapeutic target for treatment of breast cancer.