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

被引:25
作者
Li, Yijun [1 ]
Sun, Jinglu [1 ]
Cai, Yongping [1 ]
Jiang, Yan [1 ]
Wang, Xiaoqing [2 ]
Huang, Xiaojuan [1 ]
Yin, Yu [1 ]
Li, Hao [1 ]
机构
[1] Anhui Med Univ, Dept Pathol, Hefei 230032, Anhui, Peoples R China
[2] Anhui Med Coll, Dept Pathol, Hefei 230601, Anhui, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
Colorectal cancer; miR-200a; PTEN; In situ hybridization; Immunohistochemistry; EPITHELIAL-MESENCHYMAL-TRANSITION; MICRORNA EXPRESSION PROFILES; PROSTATE-CANCER PROGRESSION; HEPATOCELLULAR-CARCINOMA; DOWN-REGULATION; GENE; GROWTH; IDENTIFICATION; ASSOCIATION; METASTASIS;
D O I
10.1016/j.yexmp.2016.10.006
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
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. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:308 / 313
页数:6
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