LINC00852通过miR-625/E2F1轴调控肝细胞癌的细胞增殖、侵袭、迁移和凋亡。
LINC00852 Regulates Cell Proliferation, Invasion, Migration and Apoptosis in Hepatocellular Carcinoma the miR-625/E2F1 Axis.
作者信息
Chen Shi
机构信息
Department of Pathology, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, No. 283, Tongzipo Road, Yuelu District, Changsha, 410013 Hunan People's Republic of China.
出版信息
Cell Mol Bioeng. 2021 Dec 3;15(2):207-217. doi: 10.1007/s12195-021-00714-8. eCollection 2022 Apr.
Abstract
OBJECTIVE
This study investigates the function and regulatory mechanism of lncRNA LINC00852 in hepatocellular carcinoma (HCC) cells.
METHODS
The effects of LINC00852 and E2F1 on HCC cell proliferation, invasion, migration and apoptosis were measured by MTT assay, Transwell invasion and migration assays and TUNEL staining, respectively. The apoptosis of HCC cells was further determined by the expression levels of apoptosis-related proteins (Bax and Bcl2). Dual-luciferase reporter assays verified the targeting relationships among LINC00852, miR-625 and E2F1.
RESULTS
Overexpression of LINC00852 was positively associated with HCC cell proliferation, invasion and migration while negatively associated with the cell apoptosis. LINC00852 bound miR-625 which further targeted E2F1. Overexpressing miR-625 or down-regulating E2F1 reversed the oncogenic effects of LINC00852.
CONCLUSION
LINC00852 regulates HCC cell activities the miR-625/E2F1 axis.
摘要
目的
本研究探讨长链非编码RNA LINC00852在肝癌（HCC）细胞中的功能及调控机制。
方法
分别采用MTT法、Transwell侵袭和迁移实验以及TUNEL染色检测LINC00852和E2F1对肝癌细胞增殖、侵袭、迁移及凋亡的影响。通过凋亡相关蛋白（Bax和Bcl2）的表达水平进一步确定肝癌细胞的凋亡情况。双荧光素酶报告基因实验验证了LINC00852、miR-625和E2F1之间的靶向关系。
结果
LINC00852的过表达与肝癌细胞的增殖、侵袭和迁移呈正相关，而与细胞凋亡呈负相关。LINC00852与miR-625结合，miR-625进一步靶向E2F1。过表达miR-625或下调E2F1可逆转LINC00852的致癌作用。
结论
LINC00852通过miR-625/E2F1轴调节肝癌细胞活性。
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