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

Abstract 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.