Epigenetic silencing of miR-137 contributes to early colorectal carcinogenesis by impaired Aurora-A inhibition

Yu Chuan Huang, Chung Ta Lee, Jenq Chang Lee, Yao Wen Liu, Ying Jen Chen, Joseph T. Tseng, Jui Wen Kang, Bor Shyang Sheu, Bo Wen Lin, Liang Yi Hung

研究成果: Article同行評審

9 引文 斯高帕斯(Scopus)

摘要

MicorRNA-137 is silenced in human colorectal cancer tissues and colon polyps. Our study showed that the decreased expression of miR-137 is significantly different in various types of polyp which maintain different potentials to lead to CRC development. The expression of miR-137 gradually decreases during the process of colorectal carcinogenesis. Receiver operating characteristic curve (ROC) analysis indicates that the loss of miR-137 expression in colon polyps can serve as a biomarker to predict the predisposition of colorectal carcinogenesis. By cell model and xenograft animal model, the enforced expression of miR-137 in colorectal cancer cells can inhibit cell proliferation and tumor formation, induce G2/M arrest, and lead to apoptosis. The expression pattern of miR-137 and Aurora-A or PTGS2 is negatively correlated in human colorectal cancer tissues and colon polyps. Those effects induced by overexpressed miR-137 can be rescued by the overexpression of Aurora-A. In summary, our study suggests that the loss of miR-137 expression in colon polyps can serve as a biomarker to predict the tendency toward to CRC formation through the impaired inhibitory effect of Aurora-A. The investigation of the regulatory mechanism of miR-137-mediated Aurora-A inhibition may shed new light on the early prognosis of cancer therapy for CRC in the future.

原文English
頁(從 - 到)76852-76866
頁數15
期刊Oncotarget
7
發行號47
DOIs
出版狀態Published - 2016

All Science Journal Classification (ASJC) codes

  • 腫瘤科

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