Original Article
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jan 28, 2011; 17(4): 470-477
Published online Jan 28, 2011. doi: 10.3748/wjg.v17.i4.470
A potential oncogenic role of the commonly observed E2F5 overexpression in hepatocellular carcinoma
Yuzhu Jiang, Seon-Hee Yim, Hai-Dong Xu, Seung-Hyun Jung, So Young Yang, Hae-Jin Hu, Chan-Kwon Jung, Yeun-Jun Chung
Yuzhu Jiang, Hai-Dong Xu, Seung-Hyun Jung, So Young Yang, Hae-Jin Hu, Yeun-Jun Chung, Integrated Research Center for Genome Polymorphism and Department of Microbiology, School of Medicine, The Catholic University of Korea, Socho-gu, Seoul 137-701, South Korea
Seon-Hee Yim, Integrated Research Center for Genome Polymorphism and Department of Medical Humanities and Social Sciences, School of Medicine, The Catholic University of Korea, Socho-gu, Seoul 137-701, South Korea
Chan-Kwon Jung, Hospital Pathology, Seoul St Mary’s Hospital, Socho-gu, Seoul 137-701, South Korea
Author contributions: Chung YJ and Jiang Y designed the research; Jiang Y, Xu HD, Jung SH and Yang SY performed the experiments; Jiang Y, Yim SH and Hu HJ analyzed the data; Jung CK contributed reagents/analytic tools; Chung YJ, Jiang Y and Yim SH wrote the paper.
Supported by A grant of the Korea Healthcare technology R&D Project, Ministry of Health and Welfare, Republic of Korea (A092258) and by FG08-11-06 of the 21C Frontier Functional Human Genome Project from the Ministry of Education, Science and Technology
Correspondence to: Dr. Yeun-Jun Chung, Integrated Research Center for Genome Polymorphism and Department of Microbiology, School of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, South Korea. yejun@catholic.ac.kr
Telephone: +82-2-22587343 Fax: +82-2-5370572
Received: September 16, 2010
Revised: November 25, 2010
Accepted: December 2, 2010
Published online: January 28, 2011
Abstract

AIM: To explore the expression pattern of E2F5 in primary hepatocellular carcinomas (HCCs) and elucidate the roles of E2F5 in hepatocarcinogenesis.

METHODS: E2F5 expression was analyzed in 120 primary HCCs and 29 normal liver tissues by immunohistochemistry analysis. E2F5-small interfering RNA was transfected into HepG2, an E2F5-overexpressed HCC cell line. After E2F5 knockdown, cell growth capacity and migrating potential were examined.

RESULTS: E2F5 was significantly overexpressed in primary HCCs compared with normal liver tissues (P = 0.008). The E2F5-silenced cells showed significantly reduced proliferation (P = 0.004). On the colony formation and soft agar assays, the number of colonies was significantly reduced in E2F5-silenced cells (P = 0.004 and P = 0.009, respectively). E2F5 knockdown resulted in the accumulation of G0/G1 phase cells and a reduction of S phase cells. The number of migrating/invading cells was also reduced after E2F5 knockdown (P = 0.021).

CONCLUSION: To our knowledge, this is the first evidence that E2F5 is commonly overexpressed in primary HCC and that E2F5 knockdown significantly repressed the growth of HCC cells.

Keywords: E2F5; E2F family; Hepatocellular carcinoma; Oncogene; Small interfering RNA