Pancreatic cancer is known to be a fatal disease, which is difficult to be diagnosed in its early stages. Ubiquitin-Specific Protease
34
(USP
34
) are closely related to human cancers in the development and progression. However, there are rarely studies about the role of USP
34
in pancreatic cancer. Thus, we aimed to investigate the effect of USP
34
in human pancreatic cancer. Short-hairpin RNA targeting USP
34
(USP
34
-shRNA) and USP
34
overexpression lentivirus were used in the current study. The level of USP
34
in human pancreatic cancer (PANC-1) cells were then analyzed by quantitative (q)RT-PCR. In addition, Western blotting was used to examine phosphorylated (p)-AKT, p-protein kinase C (PKC) and p-extracellular signal-regulated kinase (ERK) protein levels. CCK-8 assay, flow cytometry, and migration assay were used to detect cell proliferation, apoptosis and migration, respectively
in vitro. According to the result of qRT-PCR and Western blotting, USP
34
-shRNA1 significantly downregulated
USP34
gene level in PANC-1 cell. Subsequently, Western blotting assay indicated that USP34
silencing significantly down-regulated the expression of p-AKT and p-PKC in cells. On the other hand, USP34
overexpressing remarkably up-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 PACN-1 cell apoptosis. Our results indicated USP34
regulated h PANC-1 cell survival via AKT and PKC pathways, and which played a pro-survival role in human pancreatic cancer. Therefore, we suggested USP34
could be a potential therapeutic target for pancreatic cancer.
抄録全体を表示