LSH promotes the growth and invasion of HCC via transcriptional regulation of CENPF expression.

LSH (lymphoid-specific helicase) is overexpressed in tumor tissues and its overexpression was associated with poor prognosis in several cancers. However, its role and molecular mechanism of LSH in hepatocellular carcinoma (HCC) remains largely unknown. Here, we report that LSH was overexpressed in tumor tissues of HCC, and overexpression of LSH was associated with poor prognosis from 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 OS and higher cumulative recurrence rates of HCC. In conclusion, LSH promotes the tumor growth of HCC through transcriptional regulation of CENPF expression, LSH may be a novel predictor for prognosis and a potential therapeutic target for HCC. This article is protected by copyright. All rights reserved.