Role of heat shock protein 27 in gemcitabine-resistant human pancreatic cancer: Comparative proteomic analyses

Abstract

The most notable obstacle hindering the effective treatment of human pancreatic cancer is intrinsic chemoresistance. In order to identify the candidate protein(s) responsible for the intrinsic chemoresistance, the protein expression profiling of human pancreatic adenocarcinoma cell line Capan-1 and its distinct surviving cells following primary treatment with gemcitabine (GEM) were compared by two-dimensional electrophoresis (2-DE) combined with liquid chromatography-mass spectrometry (LC-MS) or mass spectrometry (MS). In total, nine proteins were identified, and heat shock protein B1 (HSP27), one of the differentially expressed proteins, was selected for further validation. Furthermore, the results of western blotting and immunohistochemical staining indicated that HSP27 may be significant in pancreatic intrinsic chemoresistance to GEM. The findings of this study provide a platform for further elucidation of the underlying mechanisms of pancreatic cancer intrinsic chemoresistance and demonstrate that HSP27 may be a valid target for anticancer drug development.