Effects Of Deubiquitination Enzymes USP34 On The Proliferation,Migration And Apoptosis Of Human Pancreatic Cancer Cells

Purpose:In order to verify the effect of deubiquitination enzymes USP34 on the biological activity of human pancreatic cancer cells,we explore the expression of USP34 in human pancreatic cancer cells and investigate the effect of USP34 on pancreatic cancer cells in vitro.The purpose of this study was to provide a theoretical basis for the discovery of the role of USP34 in the diagnosis and therapy of pancreatic cancer.Methods:1.Five specimens of confirmed pancreatic cancer tissues were selected,and immunohistochemical staining was used to analyze the expression of USP34 in tumor tissues and corresponding normal tissues adjacent to the cancer.2.Human pancreatic cancer PANC-1 cells were cultured in vitro and transfected by USP34 lentivirus vector to construct stable groups according to negative control group,inhibition group,overexpression group,as long as untransfected blank group.For these groups,QRT-PCR was used to analyse the level of USP34.Additionally,in order to find the possible signaling pathways regulated by USP34,we also use western blot to examine the protein levels of AKT,PKC and ERK.3.In vitro experiments,we aim to confirm the effects of different levels of USP34 on the biological activities of pancreatic cancer cells,such as proliferation,migration,and apoptosis and identify related effective signaling pathways.Results:Our experiments confirmed that the expression of USP34 in pancreatic cancer tissues is higher than that in adjacent tissues.Gene and protein analysis showed that USP34 levels were greatly silenced or overexpressed in PANC-1 cell lines constructed by different lentivirus transfection.Further research indicated that USP34 silencing down-regulated the expression of p-AKT and p-PKC in cells.In addition,USP34 overexpression promoted PANC-1 cell proliferation and migration via up-regulating the proteins of p-AKT and p-PKC.Moreover,USP34 overexpression reversed AKT inhibitor and PKC inhibitor induced PANC-1 cell apoptosis.Conclusion:Our results indicated that USP34 regulated PANC-1 cell survival via AKT and PKC pathways and played a pro-survival role in human pancreatic cancer.Therefore,we suggested that USP34 could be a potential target for the therapy of pancreatic cancer.