LINC00963 promotes hepatocellular carcinoma progression by activating PI3K/AKT pathway

J.-H. Wu, X.-Y. Tian, Q.-M. An, X.-Y. Guan, C.-Y. Hao

Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Hepato-Pancreato-Biliary Surgery, Peking University Cancer Hospital anad Institute, Beijing, China. haochunyi@bjmu.edu.cn

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• Oncology

OBJECTIVE: To explore the role of LINC00963 in the pathogenesis of hepatocellular carcinoma and its underlying mechanisms.

PATIENTS AND METHODS: The expression level of LINC00963 in 48 cases of hepatocellular carcinoma (HCC) tissues and paracancerous tissues were detected by quantitative Real-time (qRT-PCR). Survival analysis was carried out based on the expression level of LINC00963. The association between the expression level of LINC00963 and clinical characteristics of these subjects was analyzed by x2-test. The proliferation and cell cycle of HCC cells after transfection of LINC00963 overexpression plasmids were evaluated by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively.

RESULTS: The expression level of LINC00963 in HCC tissues was remarkably higher than that in paracancerous tissues, indicating a potential diagnostic significance of LINC00963. The progression-free -with the tumor size and TNM stage, but not with age, gender, histological type and lymph node metastasis. Overexpression of LINC00963 significantly enhanced the proliferation ability of HepG2 and HCC cells and prolonged their G0/G1 phase. Furthermore, the PI3K/AKT expression was increased after overexpression of LINC00963, while AKT siRNA effectively reversed the prolonged G0/G1 phase caused by LINC00963 overexpression.

CONCLUSIONS: Our data revealed that LINC00963 was upregulated in HCC, which significantly extended the G0/G1 phase of HCC cells by activating PI3K/AKT pathway and promoting the proliferative ability of HCC cells. LINC00963 may be involved in the HCC development.

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