G Song1, Y Cui, N Zhong, J Han. 1. Shandong Medicinal Biotechnology Center, Shandong Academy of Medicinal Sciences, Key Laboratory for Biotech-Drugs Ministry of Health & Key Laboratory for Modern Medicine and Technology of Shandong Province, Jinan, Shandong Province, China.
Abstract
AIM: To characterise the protein expression profiles of pancreatic islet beta-cells affected by cancer cells, and to identify the potential islet molecules related to pancreatic cancer-associated diabetes. METHODS: The cellular proteins of islet beta-cell line INS-1 in response to conditioned medium (CM) prepared from pancreatic cancer cells were analysed using fluorescence-labelled 2D gel-based proteomics (2D-DIGE). RESULTS: 10 proteins were over-expressed and five were under-expressed in cancer CM-stimulated beta-cells. Five differently expressed proteins were selected for further validation by Western blot analysis. HSP60 and peripherin, which have previously been reported to be associated with type 1 diabetes, and Prp19, a DNA repair protein, were up-regulated in INS-1 cells after cancer cell CM stimulation; HMOX1 and GRP78 were down-regulated. The islets adjacent to human pancreatic carcinomas showed increased peripherin expression than normal pancreatic islets. CONCLUSION: These results provide new information regarding the regulation of protein expression in pancreatic cancer-associated diabetes.
AIM: To characterise the protein expression profiles of pancreatic islet beta-cells affected by cancer cells, and to identify the potential islet molecules related to pancreatic cancer-associated diabetes. METHODS: The cellular proteins of islet beta-cell line INS-1 in response to conditioned medium (CM) prepared from pancreatic cancer cells were analysed using fluorescence-labelled 2D gel-based proteomics (2D-DIGE). RESULTS: 10 proteins were over-expressed and five were under-expressed in cancer CM-stimulated beta-cells. Five differently expressed proteins were selected for further validation by Western blot analysis. HSP60 and peripherin, which have previously been reported to be associated with type 1 diabetes, and Prp19, a DNA repair protein, were up-regulated in INS-1 cells after cancer cell CM stimulation; HMOX1 and GRP78 were down-regulated. The islets adjacent to humanpancreatic carcinomas showed increased peripherin expression than normal pancreatic islets. CONCLUSION: These results provide new information regarding the regulation of protein expression in pancreatic cancer-associated diabetes.