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Oncol Rep. 2015 Aug;34(2):877-83. doi: 10.3892/or.2015.4049. Epub 2015 Jun 11.

MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer.

Author information

1
Department of General Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
2
Department of Surgery Research Laboratory, The Affiliated Hospital of Nantong University, Nantong, Jiangsu 226000, P.R. China.

Abstract

Accumulating evidence has shown that miR-196a plays an important role in tumorigenesis and tumor progression in various types of cancer. miRNA profiling studies have suggested that miR-196a is highly overexpressed in breast cancer. However, the functional mechanism of miR-196a in breast cancer remains unclear. In the present study, we first showed that the expression of miR-196a was significantly upregulated in human breast cancer samples and breast cancer cell lines. Using a loss-of-function approach, we showed that the downregulation of miR-196a inhibited the proliferation of breast cancer cells in vitro and in vivo. Ubiquitin-conjugating enzyme E2C (UBE2C) gene as a cellular proto-oncogene, which was overexpressed and positively correlated with miR-196a expression in breast cancer tissues, was identified as a direct target of miR-196a. Moreover, in order to investigate whether miR-196a regulated cell growth in breast cancer cells by targeting UBE2C, rescue studies were performed in breast cancer cells. The restoration of UBE2C by transfecting UBE2C cDNA in anti-miR-196a-transfected breast cancer cells rescued the suppression of cell proliferation. In conclusion, the present study showed that miR-196a promoted cell proliferation by targeting UBE2C in breast cancer. Thus, miR-196a may be a potential oncogene in breast cancer and a promising therapeutic target in breast cancer treatment.

PMID:
26062455
DOI:
10.3892/or.2015.4049
[Indexed for MEDLINE]

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