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Oncol Rep. 2012 Mar;27(3):807-12. doi: 10.3892/or.2011.1574. Epub 2011 Dec 1.

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1.

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Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, PR China.


It is well known that microRNAs (miRNAs) play important roles in cancer development by targeting oncogenes or tumor-suppressor genes. However, little is known regarding the mechanisms of miR-30c action in endometrial cancer. In this study, we aimed to determine whether miR-30c targets metastasis-associated gene-1 (MTA1) and acts as a tumor suppressor in endometrial cancer cell lines Ishikawa (estrogen receptor-positive, ER+) and HEC-1-B (ER-) by down-regulating MTA1. As a result, in both Ishikawa and HEC-1-B cells, real-time PCR demonstrated that overexpression of miR-30c led to the down-regulation of MTA1 mRNA (P<0.05), while Western blotting confirmed the reduced expression levels of MTA1 protein (P<0.01). A dual-luciferase reporter assay demonstrated that miR-30c was directly bound to the 3'-untranslated regions of MTA1. Then we studied the biological mechanisms of endometrial cancer cells transfected with the Pre-miR-30c plasmid. MTT assay and growth curves revealed that miR-30c inhibits both Ishikawa and HEC-1-B cell proliferation. However, we did not see obvious differences in rates of apoptosis between miR-30c-overexpressing and the negative control cells. Then using wound-healing and Matrigel invasion assays, we found that the migratory and invasive abilities of cells transfected with the Pre-miR-30c plasmid were significantly suppressed compared with the control cells (P<0.01). Overall, our study, for the first time, showed that MTA1 is negatively regulated by miR-30c and that overexpression of miR-30c inhibits the proliferative, migratory and invasive abilities of endometrial cancer cells. These results suggest that miR-30c acts as a tumor suppressor and negatively regulates endometrial cancer cells by targeting MTA1.

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