ABL1 is Overexpressed and Activated in Hepatocellular Carcinoma

Abstract

Background and Aims: ABL1 is a non-receptor tyrosine kinase of the Abelson (Abl) family, which plays an important role in cell growth, survival, invasiveness, adhesion, and migration. Despite the well-known role of BCR-ABL in hematologic malignancies, the role of ABL1 in hepatocarcinogenesis remains unknown. In this study, we want to determine if ABL1 is dysregulated in HCC. Methods: We analyzed ABL1 mRNA in two cohorts of HCC databases from Oncomine. In addition, we performed immunohistochemistry (IHC) to examine the expression of ABL1 and p-ABL1 (Y412) in HCC tissue microarray (TMA). Further, we examined ABL1 expression and activity in oncogenes cMET/β-catenin-induced mouse HCC model. Results: We found that ABL1 mRNA is overexpressed in over 50% of HCC. We also found that ABL1 protein expression is upregulated or activated in about 35% HCC specimens compared to adjacent normal liver. In addition, we found that ABL1 protein expression is upregulated and activated in cMET/β-catenin-induced HCC. Conclusion: ABL1 is overexpressed and activated in human and mouse HCC. ABL1 might be a potential therapeutic target for HCC.