Original Article
HSP27 promotes epithelial-mesenchymal transition through activation of the β-catenin/MMP3 pathway in pancreatic ductal adenocarcinoma cells
Abstract
Background: The precise role of heat shock protein 27 (HSP27), as a type of small molecular protein in HSPs, in pancreatic ductal adenocarcinoma (PDAC) remains to be elucidated. The aim of the present study was to investigate the expression and function of HSP27 in PDAC cells.
Methods: We first detected the expression of HSP27 in PDAC tissues. Combining with the clinical pathology characteristics of PDAC patients, the relationship between them was analyzed. Then, we knocked down HSP27 using short interfering RNA (siRNA) and observed its biological functions using scratch assay and matrigel invasion and migration assays in ASPC-1 and PANC-1 cells. In mechanism, we verified the β-catenin/MMP-3 pathway associated proteins in ASPC-1 and PANC-1 cells.
Results: We found that HSP27 was highly expression in PDAC tissues, and was positively correlated with tumor differentiation, TNM staging and poor prognosis of PDAC patients. In vitro, we down-regulated the expression of HSP27 in ASPC-1 and PANC-1 cells and found that the invasion and migration ability of PDAC cells were significantly depressed, meanwhile, the activation of the β-catenin/MMP-3 pathway was inhibited.
Conclusions: HSP27 may be used as a tumor biomarker for diagnosis of PDAC, and HSP27 can promote the invasion and migration of PDAC by activating the β-catenin/MMP3 Pathway. Therefore, inhibition of HSP27 has therapeutic potential for the treatment of PDAC.
Methods: We first detected the expression of HSP27 in PDAC tissues. Combining with the clinical pathology characteristics of PDAC patients, the relationship between them was analyzed. Then, we knocked down HSP27 using short interfering RNA (siRNA) and observed its biological functions using scratch assay and matrigel invasion and migration assays in ASPC-1 and PANC-1 cells. In mechanism, we verified the β-catenin/MMP-3 pathway associated proteins in ASPC-1 and PANC-1 cells.
Results: We found that HSP27 was highly expression in PDAC tissues, and was positively correlated with tumor differentiation, TNM staging and poor prognosis of PDAC patients. In vitro, we down-regulated the expression of HSP27 in ASPC-1 and PANC-1 cells and found that the invasion and migration ability of PDAC cells were significantly depressed, meanwhile, the activation of the β-catenin/MMP-3 pathway was inhibited.
Conclusions: HSP27 may be used as a tumor biomarker for diagnosis of PDAC, and HSP27 can promote the invasion and migration of PDAC by activating the β-catenin/MMP3 Pathway. Therefore, inhibition of HSP27 has therapeutic potential for the treatment of PDAC.
