Research Papers:

MicroRNA-31 functions as a tumor suppressor by regulating cell cycle and epithelial-mesenchymal transition regulatory proteins in liver cancer

Hyung Seok Kim, Kyo Sun Lee, Hyun Jin Bae, Jung Woo Eun, Qingyu Shen, Se Jin Park, Woo Chan Shin, Hee Doo Yang, Mijung Park, Won Sang Park, Yong-Koo Kang and Suk Woo Nam _

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Oncotarget. 2015; 6:8089-8102. https://doi.org/10.18632/oncotarget.3512

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Hyung Seok Kim1,2,*, Kyo Sun Lee3,*, Hyun Jin Bae1,2, Jung Woo Eun1,2, Qingyu Shen1,2, Se Jin Park1,2, Woo Chan Shin1,2, Hee Doo Yang1,2, Mijung Park1,2, Won Sang Park1,2, Yong-Koo Kang3 and Suk Woo Nam1,2,4

1 Lab of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea

2 Functional RNomics Research Center, The Catholic University of Korea, Seoul, Republic of Korea

3 Department of Orthopedic Surgery, College of Medicine, The Catholic University of Korea, Gyeonggi-do, Korea

4 Cancer Evolution Research Center, Catholic University of Korea, Seoul, Republic of Korea

* These authors contributed equally to this work

Correspondence to:

Suk Woo Nam, email:

Keywords: Hepatocellular carcinoma, microRNA-31, CDK2, HDAC2, cell cycle

Received: October 01, 2014 Accepted: February 04, 2015 Published: March 10, 2015


MicroRNA-31 (miR-31) is among the most frequently altered microRNAs in human cancers and altered expression of miR-31 has been detected in a large variety of tumor types, but the functional role of miR-31 still hold both tumor suppressive and oncogenic roles in different tumor types. MiR-31 expression was down-regulated in a large cohort of hepatocellular carcinoma (HCC) patients, and low expression of miR-31 was significantly associated with poor prognosis of HCC patients. Ectopic expression of miR-31 mimics suppressed HCC cell growth by transcriptional deregulation of cell cycle proteins. Additional study evidenced miR-31 directly to suppress HDAC2 and CDK2 expression by inhibiting mRNA translation in HCC cells. We also found that ectopic expression of miR-31 mimics reduced metastatic potential of HCC cells by selectively regulating epithelial-mesenchymal transition (EMT) regulatory proteins such as N-cadherin, E-cadherin, vimentin and fibronectin. HCC tissues derived from chemical-induced rat liver cancer models validated that miR-31 expression is significantly down-regulated, and that those cell cycle- and EMT-regulatory proteins are deregulated in rat liver cancer. Overall, we suggest that miR-31 functions as a tumor suppressor by selectively regulating cell cycle and EMT regulatory proteins in human hepatocarcinogenesis providing a novel target for the molecular treatment of liver malignancies.

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