Functional characteristics of autophagy in pancreatic cancer induced by glutamate metabolism in pancreatic stellate cells.

Abstract

ObjectiveTo observe the effects of glutaminase (GLS) inhibitors on autophagy and proliferation of pancreatic stellate cells, and to explore their functions in pancreatic cancer.MethodsPancreatic cancer cells were divided into two groups. Group A was the control untreated group, and group B cells were treated with GLS inhibitors. Western blotting was used to detect the expression of Atg5, Bcl-2, Bax, and Bid proteins. The bromodeoxyuridine assay and scratch test were employed to investigate cell proliferation and invasion, respectively. The expression of E-cadherin, vimentin, cell adhesion molecule 2 (CADM2), and Snail protein was investigated by immunofluorescence.ResultsThe expression of Atg5, Bax, and Bid was higher in group A than in group B, while Bcl-2 expression was lower in group A than in group B. Group A cells demonstrated greater proliferation and invasion than group B cells. The expression of E-cadherin was lower in group A cells than group B cells, while vimentin, CADM2, and Snail were expressed at higher levels in group A than group B cells.ConclusionThe inhibition of glutamine isozymes reduces autophagy and apoptosis in astrocytes, and inhibits pancreatic cancer cell proliferation and metastasis, while reducing their invasiveness.