Insulin promotes the proliferation and migration of pancreatic cancer cells by up-regulating the expression of PLK1 through the PI3K/AKT pathway

Pancreatic cancer has a particularly poor prognosis compared to other tumors. The peculiar hyperinsulin microenvironment of the pancreas is formed due to the endocrine secretion of islets in the pancreas. This study focused on the effect of insulin on the migration and proliferation of pancreatic cancer cells and its molecular mechanisms. We found that insulin promotes the proliferation and migration of pancreatic cancer cells. At the same time, it can up-regulate the expression of PLK1 in pancreatic cancer cells. Knocking down the expression of PLK1 in pancreatic cancer cells can inhibit the effect of insulin on the biological behavior of pancreatic cancer. In addition, we found that insulin activates the PI3K/AKT pathway in pancreatic cancer cells, and that inhibition of this pathway suppresses PLK1 expression. The PI3K/AKT inhibitor LY294002 inhibits the effects of insulin on the proliferation of pancreatic cancer cells. This study shows that insulin up-regulates PLK1 expression in pancreatic cancer cells via the PI3K/AKT pathway, which in this way enhances the migration and proliferation of pancreatic cancer cells. This may be one of the important reasons for the poor prognosis of pancreatic cancer.(c) 2023 Elsevier Inc. All rights reserved.

Automated summary

This study focuses on the role of insulin in the migration and proliferation of pancreatic cancer cells and its molecular mechanisms. It was found that insulin promotes the proliferation and migration of pancreatic cancer cells by up-regulating the expression of PLK1. Inhibition of PLK1 expression can counteract the effects of insulin on the biological behavior of pancreatic cancer cells. Additionally, insulin activates the PI3K/AKT pathway in pancreatic cancer cells, and inhibiting this pathway suppresses PLK1 expression. The findings suggest that the up-regulation of PLK1 by insulin via the PI3K/AKT pathway enhances the migration and proliferation of pancreatic cancer cells, contributing to the poor prognosis of pancreatic cancer.