Open AccessLymphoid‐specific helicase promotes the growth and invasion of hepatocellular carcinoma by transcriptional regulation of centromere protein F expression
Author(s) -
Yang Xuan,
Miao BiSi,
Wei ChuanYuan,
Dong RuiZhao,
Gao PingTing,
Zhang XinYu,
Lu JiaCheng,
Gao Chao,
Wang XiaoYing,
Sun HuiChuan,
Zhou Jian,
Fan Jia,
Ke AiWu,
Shi GuoMing,
Cai JiaBin
Publication year - 2019
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.14037
Subject(s) - hepatocellular carcinoma , ectopic expression , cancer research , rna helicase a , biology , transcription factor , helicase , gene , genetics , rna
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.