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International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

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Article

microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway

  • Authors:
    • Qunying Ma
    • Xinying Wang
    • Zhao Li
    • Bingsheng Li
    • Fengli Ma
    • Liang Peng
    • Yu Zhang
    • Angao Xu
    • Bo Jiang
  • View Affiliations / Copyright

    Affiliations: Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Huizhou Medicine Institute, Huizhou First Hospital, Huizhou 516001, P.R. China
  • Pages: 1652-1658
    |
    Published online on: January 31, 2013
       https://doi.org/10.3892/or.2013.2262
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Abstract

Dysregulated expression of microRNAs (miRNA) is a hallmark of cancer. miR-16 has been reported to be downregulated and to act as a tumor suppressor in different cancer types. In the present study, we sought to investigate the possible roles and mechanisms of miR-16 and its relationship with p53 and survivin in CRC cells. We showed that miR-16 was downregulated in 67% of CRC tissues and was correlated with the degree of histological differentiation. Experiments in vitro showed that overexpression of miR-16 inhibited the proliferation and induced apoptosis of CRC cells through the intrinsic apoptosis pathway. We further showed that miR-16 repressed survivin expression at both the mRNA and protein levels and the survivin gene was a direct target of miR-16. In addition, miR-16 reduced p53 expression and p53 increased miR-16 levels, with downregulation of miR-16 targets survivin, cyclin D1 and CDK6. Our findings suggest that miR-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway. Our findings provide further evidence for the involvement of dysregulated miRNAs in CRC, and miR-16 could serve as a molecular target for CRC therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Ma Q, Wang X, Li Z, Li B, Ma F, Peng L, Zhang Y, Xu A and Jiang B: microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway. Oncol Rep 29: 1652-1658, 2013.
APA
Ma, Q., Wang, X., Li, Z., Li, B., Ma, F., Peng, L. ... Jiang, B. (2013). microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway. Oncology Reports, 29, 1652-1658. https://doi.org/10.3892/or.2013.2262
MLA
Ma, Q., Wang, X., Li, Z., Li, B., Ma, F., Peng, L., Zhang, Y., Xu, A., Jiang, B."microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway". Oncology Reports 29.4 (2013): 1652-1658.
Chicago
Ma, Q., Wang, X., Li, Z., Li, B., Ma, F., Peng, L., Zhang, Y., Xu, A., Jiang, B."microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway". Oncology Reports 29, no. 4 (2013): 1652-1658. https://doi.org/10.3892/or.2013.2262
Copy and paste a formatted citation
x
Spandidos Publications style
Ma Q, Wang X, Li Z, Li B, Ma F, Peng L, Zhang Y, Xu A and Jiang B: microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway. Oncol Rep 29: 1652-1658, 2013.
APA
Ma, Q., Wang, X., Li, Z., Li, B., Ma, F., Peng, L. ... Jiang, B. (2013). microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway. Oncology Reports, 29, 1652-1658. https://doi.org/10.3892/or.2013.2262
MLA
Ma, Q., Wang, X., Li, Z., Li, B., Ma, F., Peng, L., Zhang, Y., Xu, A., Jiang, B."microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway". Oncology Reports 29.4 (2013): 1652-1658.
Chicago
Ma, Q., Wang, X., Li, Z., Li, B., Ma, F., Peng, L., Zhang, Y., Xu, A., Jiang, B."microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway". Oncology Reports 29, no. 4 (2013): 1652-1658. https://doi.org/10.3892/or.2013.2262
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