Objective: To explore the expression and biological function of protocadherin 10 (PCDH10) in pancreatic cancer cells.
Methods: Reverse transcription PCR (RT-PCR) was used to detect the expression of PCDH10 in CAPAN-1, PANC-1, ASPC-1, BXPC-3 pancreatic cancer cells and the HPDE6-C7 normal human pancreatic ductal epithelial cells. Recombinant plasmid pcDNA3.1-PCDH10 and empty vector pcDNA3.1 were transfected into BXPC-3 pancreatic cancer cells via Lipofectamine(TM)2000. After transfection, the mRNA expression of PCDH10 was examined by RT-PCR, and the protein level was detected by Western blotting. CCK-8 and colony formation assays were used to analyze the cell proliferation. Cell apoptosis was tested by flow cytometry combined with annexin V-FITC/PI staining. Transwell(TM) and wound healing assays were performed to measure the invasion and migration ability of the cells.
Results: Compared with the normal pancreatic ductal epithelial cells, the expression of PCDH10 was obviously lower in the CAPAN-1, PANC-1, BXPC-3 cells. RT-PCR and Western blotting revealed that PCDH10 expression significantly increased in BXPC-3 cells transfected with plasmid pcDNA3.1-PCDH10 compared with the ones with empty vector pcDNA3.1. CCK-8 and colony formation assays showed that the PCDH10-transfected cells grew more slowly than the empty vector-transfected cells. Annexin V-FITC/PI staining combined with flow cytometry proved that the apoptosis in the PCDH10-transfected cells remarkably increased compared with that in the control group. A reduction of the invasion and migration ability was found obviously in the PCDH10-transfected cells by Transwell(TM) assay. The wound healing assay also showed that the PCDH10-transfected cells spread the more slowly than the empty vector-transfected cells.
Conclusion: The expression of PCDH10 was down-regulated in the pancreatic cancer cells. PCDH10 over-expression could significantly induce cell apoptosis, and restrain proliferation, invasion and migration ability of BXPC-3 pancreatic cancer cells.