胰腺癌
PI3K/AKT/mTOR通路
癌症研究
蛋白激酶B
胰腺
癌细胞
胰岛素
癌症
内科学
内分泌学
生物
化学
细胞生物学
信号转导
医学
作者
Kaichun Wu,Hao Chen,Yue Fu,Xiang Cao,Chunzhao Yu
标识
DOI:10.1016/j.bbrc.2023.01.061
摘要
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.
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