Objective  To explore the function and mechanism of protein kinase CβⅡ(PKCβⅡ) in the progression of hepatocellular carcinoma(HCC).   Methods  The expression of PKCβⅡ in hepatic cell L02 and HCC cell lines (SK-hep1, HepG2, BEL-7404, 7721, Hep3B and huh7)was examined by Western blotting. Stable HCC cells over-expressing PKCβⅡ were constructed, the morphological change was observed under inverted phase microscope, immunofluorescence was applied to examine the expression of E-cadherin and N-cadherin. Western blotting, Real-time PCR and cycloheximide (CHX) chase assay were used to examine the molecular mechanism of PKCβⅡ in modulating the expression of  E-cadherin, N-cadherin and Snail. The effect of PKCβⅡ on the metastasis of HCC was examined by using transwell assay and nude mice tail vein injection. Tube formation assay was used to detect the impact of PKCβⅡ on the tube formation by human umbilical vein endothelial cells(HUVECs), enzyme linked immunosorbent assay(ELISA) was used to detect the impact of PKCβⅡ on the content of vascular endothelical growth factor(VEGF)A in the supernatant of HCC cells.   Results  The expression of PKCβⅡ in HCC cells was higher than that in hepatic cell L02, PKCβⅡ promoted the morphologic phenotype changed from cobblestone-like epithelial cells to spindle-shaped mesenchymal-like cells, with the expression of E-cadherin down-regulated（P<0.05）and N-cadherin up-regulated（P<0.01） at mRNA level, as well as Snail up-regulated at translation level. Meanwhile, PKCβⅡ improved migratory and invasive abilities（P<0.01）of HCC cells as well as VEGFA secretion（P<0.01）and angiogenesis（P<0.01）.   Conclusion  Protein kinase CβⅡ promotes the development of hepatocellular carcinoma via inducing epithelial-mesenchymal transition and angiogenesis.