Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most deadly cancers in the world and hyperinsulinemia has been considered to be associated with the risk of pancreatic cancer. Our study is to explore the effect of insulin on the migration and invasion of pancreatic cancer cells and possible mechanism. Results: Insulin could enhance the invasion and migration of pancreatic cancer cells through the transwell assay. Insulin receptor (INSR) is the major membrane receptor in this process. Based on digital gene expression sequencing and cell line confirmation, formin homology 2 domain containing protein 1 (FHOD1) was determined to be positively involved in insulin-induced migration and invasion. In addition, insulin and the downstream molecule FHOD1 could promote epithelial-mesenchymal transition in pancreatic cancer cells, which may subsequently promote malignant biological behaviour. Conclusion: We reported that INSR is the major receptor involved in insulin-induced pancreatic cell mobility alterations. Epithelial-mesenchymal transition, which was regulated through FHOD1, participated in this INSR-dependent phenotypic modification. This study provided a theoretical explanation for previous epidemiological research and new clues for further exploration of the diagnosis and treatment of T2DM pancreatic cancer patients.
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