Abstract
IntroductionAbl2 nonreceptor tyrosine kinase (Arg, c-abl oncogene 2) has recently been identified as being recurrently amplified at DNA levels and overexpressed at mRNA levels in hepatocellular carcinomas (HCCs), and might be a potential oncogenic driver and therapeutic target for HCC.MethodsIn this study, we investigated the Abl2 expression in a series of HCC tumors by immunohistochemistry and further evaluated its clinicopathological and prognostic significance. We also performed an in vitro experiment to validate the effect of Abl2 gene silencing on the migration and invasion abilities of human liver cancer HepG2 cells.ResultsIt has been demonstrated that Abl2 was unregulated in 37.3% (28/75) of primary HCC tissues, and was significantly associated with a shorter overall survival time (P=0.0005). In addition, Abl2 gene silencing in HepG2 cells significantly attenuated its migration and invasion abilities in vitro. We also found that the phosphorylation of metastasis-associated gene cortactin was markedly decreased by Abl2 silencing.ConclusionWe propose that Abl2 might be a potential candidate therapeutic target for HCCs and that targeted therapies against Abl2 in the treatment of HCCs deserve further investigation in the future.
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