Lymphoid‐specific helicase promotes the growth and invasion of hepatocellular carcinoma by transcriptional regulation of centromere protein F expression. Issue 7 (25th May 2019)

• Record Type: Journal Article
• Authors: Yang, Xuan; Miao, Bi‐Si; Wei, Chuan‐Yuan; Dong, Rui‐Zhao; Gao, Ping‐Ting; Zhang, Xin‐Yu; Lu, Jia‐Cheng; Gao, Chao; Wang, Xiao‐Ying; Sun, Hui‐Chuan; Zhou, Jian; Fan, Jia; Ke, Ai‐Wu; Shi, Guo‐Ming; Cai, Jia‐Bin
• Is Part Of: Cancer science. Volume 110:Issue 7(2019)
• Page Start: 2133
• Page End: 2144
• Publication Date: 2019-05-25
• Subjects: CENPF -- ChIP‐seq -- HCC -- LSH -- RNA‐seq; Cancer -- Periodicals; Neoplasms -- Periodicals; Research -- Periodicals; Electronic journals; 616.994005
• DOI: 10.1111/cas.14037
• Languages: English
• ISSNs: 1347-9032

Abstract

Abstract: Lymphoid‐specific helicase (LSH) is overexpressed in tumor tissues and its overexpression is associated with poor prognosis in several cancers. However, the role and molecular mechanism of LSH in hepatocellular carcinoma (HCC) remains largely unknown. Herein, we report that LSH was overexpressed in tumor tissues of HCC, and overexpression of LSH was associated with poor prognosis from a public HCC database, and validated by clinical samples from our department. Ectopic LSH expression promoted the growth of HCC cells in vivo and in vitro. Mechanistically, LSH overexpression promoted tumor growth by activating transcription of centromere protein F (CENPF). Clinically, overexpression of LSH and/or CENPF correlated with shorter overall survival and higher cumulative recurrence rates of HCC. In conclusion, LSH promotes tumor growth of HCC through transcriptional regulation of CENPF expression. Therefore, LSH may be a novel predictor for prognosis and a potential therapeutic target for HCC. Abstract : In the present study, we first evaluated LSH as a potential prognostic marker in hepatocellular carcinoma. We also investigated the cellular and molecular mechanism, especially in cancer invasion and metastasis. Herein, we initially determined a novel mechanism involving protein‐DNA binding between LSH and the CENPF gene.