title: microRNA-30c negatively regulates endometrial cancer cells by targeting             metastasis-associated gene-1.
abstract: 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.
authors.affiliation: Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, PR China.
authors.forename: Huaijun
authors.initials: H
authors.lastname: Zhou
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Xu
authors.forename: Qingying
authors.initials: Q
authors.lastname: Xun
authors.forename: Dongqi
authors.initials: D
authors.lastname: Yu
authors.forename: Jingxian
authors.initials: J
authors.lastname: Ling
authors.forename: Feifei
authors.initials: F
authors.lastname: Guo
authors.forename: Yuhua
authors.initials: Y
authors.lastname: Yan
authors.forename: Jiayu
authors.initials: J
authors.lastname: Shi
authors.forename: Yali
authors.initials: Y
authors.lastname: Hu
mesh_terms: D020413:3' Untranslated Regions; D017209:Apoptosis / Q000235:genetics; D048708:Cell Growth Processes / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D015536:Down-Regulation; D016889:Endometrial Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006655:Histone Deacetylases / Q000378:metabolism*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D012333:RNA, Messenger / Q000235:genetics; D012097:Repressor Proteins / Q000378:metabolism*; D015534:Trans-Activators
chemical_list: D020413:3' Untranslated Regions; C546086:MIRN30b microRNA, human; D035683:MicroRNAs; C089320:MTA1 protein, human; D012333:RNA, Messenger; D012097:Repressor Proteins; D015534:Trans-Activators; D006655:Histone Deacetylases