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Article

Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer

  • Authors:
    • Yu Zhang
    • Xinying Wang
    • Binghong Xu
    • Baocai Wang
    • Zhongqiu Wang
    • Yan Liang
    • Jieqiong Zhou
    • Jingjing Hu
    • Bo Jiang
  • View Affiliations / Copyright

    Affiliations: Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nangfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
  • Pages: 1976-1984
    |
    Published online on: July 23, 2013
       https://doi.org/10.3892/or.2013.2633
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Abstract

microRNAs (miRNAs) have been reported to play a crucial role in regulating a variety of genes pivotal for tumor metastasis. miR-126 is well known as one of the angiogenesis regulatory miRNAs. Recent studies have reported controversial roles of miR-126 in tumor progression. In this study, we sought to investigate the potential roles of miR-126 in colorectal cancer (CRC). By real-time PCR, miR-126 was shown to be downregulated in primary CRC tissues and cell lines. Restoration of miR-126 in CRC cells inhibited cell growth, migration and invasion. Using both in silico prediction and immunoblotting, we found that vascular endothelial growth factor (VEGF) was a target of miR-126. The interaction of miR-126 on the 3'UTR of VEGF mRNA was validated by luciferase reporter assay. Mechanistically, we found that the silencing of miR-126 was induced by promoter methyl­ation of its host gene, EGFL7. Treatment with 5-aza-CdR restored miR-126 expression and thereby led to a decline in VEGF expression. Functionally, due to suppression of VEGF, enhanced miR-126 expression inhibited tumor neovasculature triggered by CRC cells. In conclusion, our findings suggest that DNA methylation-induced silencing of miR-126 contributes, at least in part, to tumor invasion and angiogenesis in CRC, through upregulation of VEGF expression. miR-126 may be a potential target for the therapeutic strategy against CRC.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang Y, Wang X, Xu B, Wang B, Wang Z, Liang Y, Zhou J, Hu J and Jiang B: Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer. Oncol Rep 30: 1976-1984, 2013.
APA
Zhang, Y., Wang, X., Xu, B., Wang, B., Wang, Z., Liang, Y. ... Jiang, B. (2013). Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer. Oncology Reports, 30, 1976-1984. https://doi.org/10.3892/or.2013.2633
MLA
Zhang, Y., Wang, X., Xu, B., Wang, B., Wang, Z., Liang, Y., Zhou, J., Hu, J., Jiang, B."Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer". Oncology Reports 30.4 (2013): 1976-1984.
Chicago
Zhang, Y., Wang, X., Xu, B., Wang, B., Wang, Z., Liang, Y., Zhou, J., Hu, J., Jiang, B."Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer". Oncology Reports 30, no. 4 (2013): 1976-1984. https://doi.org/10.3892/or.2013.2633
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang Y, Wang X, Xu B, Wang B, Wang Z, Liang Y, Zhou J, Hu J and Jiang B: Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer. Oncol Rep 30: 1976-1984, 2013.
APA
Zhang, Y., Wang, X., Xu, B., Wang, B., Wang, Z., Liang, Y. ... Jiang, B. (2013). Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer. Oncology Reports, 30, 1976-1984. https://doi.org/10.3892/or.2013.2633
MLA
Zhang, Y., Wang, X., Xu, B., Wang, B., Wang, Z., Liang, Y., Zhou, J., Hu, J., Jiang, B."Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer". Oncology Reports 30.4 (2013): 1976-1984.
Chicago
Zhang, Y., Wang, X., Xu, B., Wang, B., Wang, Z., Liang, Y., Zhou, J., Hu, J., Jiang, B."Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer". Oncology Reports 30, no. 4 (2013): 1976-1984. https://doi.org/10.3892/or.2013.2633
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