MiR-200a acts as an oncogene in colorectal carcinoma by targeting PTEN

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• 作者：Yijun Li^a ; ¹ ; Jinglu Sun^a ; ¹ ; Yongping Cai^a ; Yan Jiang^a ; Xiaoqing Wang^b ; Xiaojuan Huang^a ; Yu Yin^a ; ^{aydyinyu@aliyun.com} ; Hao Li^a ; ^{Lihao3402@aliyun.com}
• 关键词：Colorectal cancer ; miR-200a ; PTEN ; In situ hybridization ; Immunohistochemistry
• 刊名：Experimental and Molecular Pathology
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：101
• 期：3
• 页码：308-313
• 全文大小：903 K
• 卷排序：101

文摘

The expression pattern of miR-200a in different types of cancer is diverse, and its mechanism in tumorigenesis has yet to be elucidated. In this study, miR-200a was significantly upregulated in the cancer tumor tissues of colorectal cancer (CRC) patients, and its expression was positively correlated with the degree of tumor differentiation. Overexpression of miR-200a enhanced cell proliferation, migration, and invasion. To understand the potential mechanism of miR-200a in tumorigenesis, we showed that miR-200a directly targeted phosphatase and tensin homolog (PTEN). To test the clinical relevance of these results, we used 107 pairs of CRC and adjacent normal tissues, analyzed miR-200a levels and PTEN expression in these tissues, and found that miR-200a levels were significantly inversely correlated with PTEN levels in the cancer tissues. These results suggest that miR-200a plays an oncogene role by regulating PTEN signaling in CRC. Our findings present important implications for further understanding the signaling mechanisms involved in modulating CRC tumorigenesis.