LINC00265 promotes the metastasis and progression of hepatocellular carcinoma by interacting with E2F1 at the promoter of CDK2

This study is aimed to explore the biological function of long intergenic non-protein coding RNA 265 (LINC00265) in hepatocellular carcinoma (HCC) cells, and evaluate its potential as a biomarker. GEPIA database and Kaplan-Meier Plotter database were employed to analyze LINC00265 expression in HCC tissue samples and its predicting value for prognosis. LINC00265 expression in HCC tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). After LINC00265 was overexpressed and knocked down in HCC cells, cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assays were adopted to detect the proliferation of HCC cells. Transwell assay was used to detect the migration and invasion of HCC cells. The interaction between LINC00265 and E2F transcription factor 1 (E2F1) was verified by the catRAPID online analysis tool, RNA pull-down experiment, and RNA binding protein immunoprecipitation (RIP) assay. The binding of E2F1 to the promoter region of cyclin-dependent kinases 2 (CDK2) was detected by dual-luciferase reporter assay and chromatin immunoprecipitation. The regulatory effects of LINC00265 and E2F1 on CDK2 expression were probed by Western blot. LINC00265 expression was increased in HCC tissues and cells. LINC00265 overexpression promoted the proliferation, migration, and invasion of HCC cells, and knocking down LINC00265 worked oppositely. LINC00265 could bind to E2F1, and LINC00265 could enhance the combination of E2F1 and CDK2 promoter regions, thus promoting CDK2 transcription. LINC00265 overexpression promoted the expression of CDK2 in HCC cells. Our data suggest that LINC00265 can promote the malignant behaviors of HCC cells by recruiting E2F1 to the promoter region of CDK2.