miR-497 induces apoptosis of breast cancer cells by targeting Bcl-w

Shen,Lei; Li,Jia; Xu,Liping; Ma,Jie; Li,Hua; Xiao,Xigang; Zhao,Junyong; Fang,Lin

doi:10.3892/etm.2011.428

March 2012 Volume 3 Issue 3

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March 2012 Volume 3 Issue 3

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Article

miR-497 induces apoptosis of breast cancer cells by targeting Bcl-w

Authors:
- Lei Shen
- Jia Li
- Liping Xu
- Jie Ma
- Hua Li
- Xigang Xiao
- Junyong Zhao
- Lin Fang
View Affiliations / Copyright

Affiliations: Department of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, P.R. China, Department of General Surgery, Ningbo First Hospital, College of Medicine, Tongji University, Shanghai, P.R. China, Department of General Surgery, Ningbo Second Hospital, College of Medicine, Tongji University, Shanghai, P.R. China
Pages: 475-480
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Published online on: December 22, 2011

https://doi.org/10.3892/etm.2011.428
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Abstract

microRNAs are a small class of non-coding RNAs with a critical role in the tumorigenesis and maintenance of breast cancer through binding to the 3'‑untranslated regions of target mRNAs, which causes a block of translation and/or mRNA degradation. The purpose of this study was to investigate the expression of microRNA-497 (miR-497) as well as its potential role in human breast cancer. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to determine the expression pattern of miR-497 in breast cancer and normal breast tissues. Correlation analysis was conducted to characterize the association of miR-497 expression abnormality with pathological factors. Proliferation, cell cycle and apoptosis assays were conducted to explore the potential function of miR-497 in human MCF-7 breast cancer cells. RT-PCR and Western blot analysis were employed to validate the downstream targets of miR-497. miR-497 expression was relatively decreased in breast cancer specimens and negatively correlated with TNM stage, lymphatic metastasis, tumor size and human epidermal growth factor receptor-2 (P<0.01). On the contrary, no correlation was found with estrogen receptor, progesterone receptor and p53 status. Functional assays revealed that miR-497 suppressed cellular growth, increased the percentage of early apoptotic cells and initiated G0/G1 cell phase arrest of MCF-7 cancer cells. RT-PCR and Western blot analysis data indicated that the overexpression of miR-497 resulted in the down‑regulation of Bcl-w at the mRNA and protein levels. miR-497 may serve as a tumor suppressor gene in breast cancer. The Up-regulation of miR-497 expression causes cellular growth inhibition and apoptotic enhancement, as well as G0/G1 phase arrest, suggesting its use as a potential therapeutic target for the treatment of breast cancer in the future.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

miR-497 induces apoptosis of breast cancer cells by targeting Bcl-w

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