Abstract
The effects of long intergenic non-coding ribonucleic acid (lincRNA)-p21 targeting hypoxia-inducible factor-1α (HIF-1α) on proliferation, apoptosis and migration of liver cancer cells were investigated. MHCC97H liver cancer cells were infected with control lentivirus (control group) and lincRNA-p21 lentivirus (observation group), and control stable cell lines and lincRNA-p21 stable cell lines were screened and obtained by using puromycin. The expression levels of lincRNA-p21 messenger RNA (mRNA) in the control and observation groups were analyzed via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Bioinformatics was used to search for the lincRNA-p21 target. The expression of target gene was analyzed via western blotting, and the proliferation, apoptosis, migration and in vivo tumor formation of MHCC97H cells in the control and observation groups were also analyzed. Compared with that in control group, the lincRNA-p21 mRNA level in observation group was increased significantly (P<0.05). It was found via bioinformatic comparison that HIF-1α was one of the targets of lincRNA-p21. Results of Western blotting revealed that the expression level of HIF-1α protein in cells in observation group was significantly downregulated (P<0.05). Besides, the level of vascular endothelial growth factor (VEGF) protein in cells in control group was obviously higher than that in observation group (P<0.05). Compared with those in control group, the cell proliferation and migration capacities in observation group were markedly reduced, but the apoptosis level was significantly increased (P<0.05). According to the in vivo tumor formation assay, the cell proliferation rate in control group was obviously higher than that in observation group (P<0.05). The number of tumor blood vessels in cells in control group was obviously reduced compared with that in observation group (P<0.05). lincRNA-p21 can significantly downregulate the level of HIF-1α, thus downregulating the expression of VEGF and affecting the cell proliferation, apoptosis and migration.