作者: Hyung Seok Kim , Kyo Sun Lee , Hyun Jin Bae , Jung Woo Eun , Qingyu Shen
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摘要: // Hyung Seok Kim 1,2,* , Kyo Sun Lee 3,* Hyun Jin Bae 1,2 Jung Woo Eun Qingyu Shen Se Park Chan Shin Hee Doo Yang Mijung Won Sang Yong-Koo Kang 3 and Suk Nam 1,2,4 1 Lab of Oncogenomics, Department Pathology, College Medicine, The Catholic University Korea, Seoul, Republic Korea 2 Functional RNomics Research Center, Orthopedic Surgery, Gyeonggi-do, 4 Cancer Evolution * These authors contributed equally to this work Correspondence to: Nam, email: Keywords : Hepatocellular carcinoma, microRNA-31, CDK2, HDAC2, cell cycle Received October 01, 2014 Accepted February 04, 2015 Published March 10, Abstract MicroRNA-31 (miR-31) is among the most frequently altered microRNAs in human cancers expression miR-31 has been detected a large variety tumor types, but functional role still hold both suppressive oncogenic roles different types. MiR-31 was down-regulated cohort hepatocellular carcinoma (HCC) patients, low significantly associated with poor prognosis HCC patients. Ectopic mimics suppressed growth by transcriptional deregulation proteins. Additional study evidenced directly suppress HDAC2 CDK2 inhibiting mRNA translation cells. We also found that ectopic reduced metastatic potential cells selectively regulating epithelial-mesenchymal transition (EMT) regulatory proteins such as N-cadherin, E-cadherin, vimentin fibronectin . tissues derived from chemical-induced rat liver cancer models validated down-regulated, those cycle- EMT-regulatory are deregulated cancer. Overall, we suggest functions suppressor EMT hepatocarcinogenesis providing novel target for molecular treatment malignancies.