MicroRNA‑185 inhibits proliferation by targeting c‑Met in human breast cancer cells

Fu,Peifen; Du,Feiya; Yao,Minya; Lv,Kezhen; Liu,Yu

doi:10.3892/etm.2014.1999

MicroRNA‑185 inhibits proliferation by targeting c‑Met in human breast cancer cells

Authors:
- Peifen Fu
- Feiya Du
- Minya Yao
- Kezhen Lv
- Yu Liu
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Affiliations: Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310003, P.R. China, Department of Plastic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310003, P.R. China
Published online on: September 30, 2014 https://doi.org/10.3892/etm.2014.1999
Pages: 1879-1883

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Abstract

MicroRNAs (miRNAs) are a group of small non‑coding RNA molecules that have been shown to regulate the expression of genes involved in tumorigenesis. The relevance of miRNAs in the development, progression and prognosis of human breast cancer is not fully understood. miR‑185 has been demonstrated to be involved in the pathogenesis of several types of cancers; however, its role in breast cancer has not yet been elucidated. In the present study, the expression of miR‑185 was analyzed by quantitative polymerase chain reaction. In addition, an MTT assay and flow cytometry were used to determine the rates of cell proliferation and apoptosis. Protein expression was analyzed by western blotting and the target gene was confirmed using a luciferase reporter assay. The expression of miR‑185 was found to be downregulated in the breast cancer tissues. The MTT assay revealed that overexpression of miR‑185 inhibited the proliferation of MDF7 and SKBR3 cells. Furthermore, flow cytometric analysis demonstrated that increased expression levels of miR‑185 promoted the apoptosis of breast cancer cells. In addition, c‑Met expression was demonstrated to be significantly upregulated in breast cancer tissues and cells, and the c‑Met gene was identified to be a target of miR‑185. Therefore, the results demonstrated that miR‑185 inhibited the proliferation of breast cancer cells by regulating the expression of c‑Met, indicating its potential as a therapeutic target for breast cancer.

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