期刊
CANCER RESEARCH
卷 79, 期 3, 页码 572-584出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-18-0367
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资金
- National Natural Science Foundation of China [81802812]
- Natural Science Foundation of Guangdong Province [2018A030313129]
- Hunan Provincial Innovation Foundation for Postgraduates [CX2016B056]
- Open-End Fund for the Valuable and Precision Instruments of Central South University [CSUZC201746]
- Fundamental Research Funds for the Central Universities of Central South University [2015zzts096]
- Science and Technology Department Research Foundation of Hunan province [12JJ2052]
Hepatocellular carcinoma (HCC) is one of the most dominant causes of neoplasm-related deaths worldwide. In this study, we identify and characterize HCCL5, a novel cytoplasmic long noncoding RNA (lncRNA), as a crucial oncogene in HCC. HCCL5 promoted cell growth, G(1)-S transition, invasion, and metastasis while inhibiting apoptosis of HCC cells both in vitro and in vivo. Moreover, HCCL5 was upregulated in TGF-beta 1-induced classical epithelial-to-mesenchymal transition (EMT) models, and this lncRNA in turn accelerated the EMT phenotype by upregulating the expression of transcription factors Snail, Slug, ZEB1, and Twist1. HCCL5 was transcriptionally driven by ZEB1 via a super-enhancer and was significantly and frequently overexpressed in human HCC tissues, correlating with worse overall survival of patients with HCC. Together, this study characterizes HCCL5 as a super-enhancer-driven lncRNA promoting HCC cell viability, migration, and EMT. Our data also suggest that HCCL5 may serve as a novel prognostic biomarker and therapeutic target in HCC. Significance: These findings identify the lncRNA HCCL5 as a super-enhancer-driven oncogenic factor that promotes the malignancy of hepatocellular carcinoma.
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