Effect of KIF2C on the malignant biological behavior of hepatocellular carcinoma cells and angiogenesis of human umbilical vein endothelial cells.

Objective: To explore the effects of kinesin-13 family member 2C (KIF2C) on hepatocellular carcinoma (HCC) cell proliferation, invasion and migration as well as human umbilical vein endothelial cell (HUVEC) angiogenesis to provide potential targets for HCC treatment. Methods: Database data were used to analyze the expression of KIF2C mRNA and protein in HCC tissues and its correlation with the expression of angiogenesis-associated factors (VEGFR2 and HIF-1α). Human normal hepatocytes QSG-7701, HUVEC, and HCC cells Huh-7 and Hep3B2.1-7 were routinely cultured, and sh-NC and sh KIF2C were transfected into Huh-7 and Hep3B2.1-7 cells with Lipofectamine 3000 transfection reagent. qPCR was performed to detect the expression of KIF2C mRNA in QSG-7701, Huh-7 and Hep3B2.1-7 cells of each group, and WB was performed to detect the expression of KIF2C protein in cells of each group, and the effect of KIF2C knockdown on the clone formation of Huh3B2.1-7 and Huh-7 cells was examined in the clonogenic assay. Tubulogenesis assay to detect the effect of conditioned cultures of knockdown KIF2C-expressing Huh-7 and Hep3B2.1-7 cells on the angiogenic capacity of HUVEC cells. Results: Database analysis showed that KIF2C mRNA and protein were highly expressed in HCC tissues (both P<0.01). In addition, database analysis suggested that KIF2C mRNA may also be highly expressed in HCC cells, and the results of KIF2C mRNA and protein expression detected by qPCR and WB showed that its mRNA and protein were highly expressed in HCC cells (both P<0.01), consistent with the database data analysis. Database data analysis also showed that KIF2C was positively correlated with the expression levels of VEGFR2 and HIF-1α in HCC tissues (P<0.05 or P<0.01). Stable low KIF2C-expressing Huh-7 and Hep3B2.1-7 cells were successfully constructed (both P<0.01), and knockdown of KIF2C expression significantly inhibited the proliferative (all P<0.01), invasive and migratory (all P<0.01) capacities of Huh-7 and Hep3B2.1-7 cells, and the conditioned culture medium of HCC cells with knockdown of KIF2C expression could significantly inhibit the angiogenic capacity of HUVEC cells in vitro (P<0.05 or P<0.01). Conclusion: KIF2C promotes the ability of Huh-7 and Hep3B2.1-7 cells to proliferate, invade and migrate as well as HUVEC angiogenesis, suggesting that KIF2C may be a potential target for the treatment of HCC. [ABSTRACT FROM AUTHOR]