Zhiming Wang1, Qingtao Zou2, Mu Song3, Jing Chen3. 1. Department of Hepatobiliary Surgery, Xiangya Hospital, Central South University, Changsha, China. Electronic address: zhimingw1@126.com. 2. Department of Hepatobiliary Surgery, Xiangya Hospital, Central South University, Changsha, China. 3. Department of General Surgery, The Second Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Abstract
BACKGROUND: Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) was found to be participated in tumorigenesis in various cancers including hepatocellular carcinoma (HCC). However, the clinical implication and underling function of NEAT1 in HCC have not been fully known. METHODS: The relative NEAT1 expression was examined by qRT-PCR in HCC tissues and cells, compared with adjacent normal tissues and normal human hepatocyte (LO2) cells, respectively. Cell proliferation and invasion were examined by MTT, cell colony formation and transwell assays. Luciferase reporter assay was performed to verify miR-613 was a direct target of NEAT1. Western blot analysis was also performed. RESULTS: NEAT1 was notably upregulated in HCC tissues and cells. Higher NEAT1 expression associated with larger tumor size and vascular invasion of HCC patients. Knockdown of NEAT1 significantly suppressed HCC cell proliferation, colony formation and cell invasion. Interestingly, lower miR-613 expression negatively associated with the NEAT1 expression in HCC tissues and was regulated by NEAT1. Additionally, we demonstrated that NEAT1 promoted HCC cell proliferation and invasion by regulating miR-613 expression. CONCLUSION: These results implied that inhibition of NEAT1 may be a potential therapeutic strategy for HCC patients.
BACKGROUND: Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) was found to be participated in tumorigenesis in various cancers including hepatocellular carcinoma (HCC). However, the clinical implication and underling function of NEAT1 in HCC have not been fully known. METHODS: The relative NEAT1 expression was examined by qRT-PCR in HCC tissues and cells, compared with adjacent normal tissues and normal human hepatocyte (LO2) cells, respectively. Cell proliferation and invasion were examined by MTT, cell colony formation and transwell assays. Luciferase reporter assay was performed to verify miR-613 was a direct target of NEAT1. Western blot analysis was also performed. RESULTS:NEAT1 was notably upregulated in HCC tissues and cells. Higher NEAT1 expression associated with larger tumor size and vascular invasion of HCC patients. Knockdown of NEAT1 significantly suppressed HCC cell proliferation, colony formation and cell invasion. Interestingly, lower miR-613 expression negatively associated with the NEAT1 expression in HCC tissues and was regulated by NEAT1. Additionally, we demonstrated that NEAT1 promoted HCC cell proliferation and invasion by regulating miR-613 expression. CONCLUSION: These results implied that inhibition of NEAT1 may be a potential therapeutic strategy for HCC patients.
Authors: Manuela Lanzafame; Gaia Bianco; Luigi M Terracciano; Charlotte K Y Ng; Salvatore Piscuoglio Journal: Int J Mol Sci Date: 2018-02-28 Impact factor: 5.923