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Article

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

  • Authors:
    • Qinglin Han
    • Chun Zhou
    • Fan Liu
    • Guanghuan Xu
    • Rui Zheng
    • Xin Zhang
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China, Department of Surgery Research Laboratory, The Affiliated Hospital of Nantong University, Nantong, Jiangsu 226000, P.R. China
  • Pages: 877-883
    |
    Published online on: June 11, 2015
       https://doi.org/10.3892/or.2015.4049
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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-tranfected 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.
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Copy and paste a formatted citation
Spandidos Publications style
Han Q, Zhou C, Liu F, Xu G, Zheng R and Zhang X: MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer. Oncol Rep 34: 877-883, 2015.
APA
Han, Q., Zhou, C., Liu, F., Xu, G., Zheng, R., & Zhang, X. (2015). MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer. Oncology Reports, 34, 877-883. https://doi.org/10.3892/or.2015.4049
MLA
Han, Q., Zhou, C., Liu, F., Xu, G., Zheng, R., Zhang, X."MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer". Oncology Reports 34.2 (2015): 877-883.
Chicago
Han, Q., Zhou, C., Liu, F., Xu, G., Zheng, R., Zhang, X."MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer". Oncology Reports 34, no. 2 (2015): 877-883. https://doi.org/10.3892/or.2015.4049
Copy and paste a formatted citation
x
Spandidos Publications style
Han Q, Zhou C, Liu F, Xu G, Zheng R and Zhang X: MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer. Oncol Rep 34: 877-883, 2015.
APA
Han, Q., Zhou, C., Liu, F., Xu, G., Zheng, R., & Zhang, X. (2015). MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer. Oncology Reports, 34, 877-883. https://doi.org/10.3892/or.2015.4049
MLA
Han, Q., Zhou, C., Liu, F., Xu, G., Zheng, R., Zhang, X."MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer". Oncology Reports 34.2 (2015): 877-883.
Chicago
Han, Q., Zhou, C., Liu, F., Xu, G., Zheng, R., Zhang, X."MicroRNA-196a post-transcriptionally upregulates the UBE2C proto-oncogene and promotes cell proliferation in breast cancer". Oncology Reports 34, no. 2 (2015): 877-883. https://doi.org/10.3892/or.2015.4049
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