Fyn stimulates the progression of pancreatic cancer via Fyn-GluN2b-AKT axis.

Abstract

To assess the expression levels of Fyn in human tissue samples and pancreatic cancer cells and explore the potential mechanisms of Fyn in pancreatic cancer progression. Quantitative PCR and immunohistochemical (IHC) assays were performed to detect the expression of Fyn in 30 cancer tissue samples from pancreatic cancer patients and corresponding adjacent normal tissues. In addition, the potential correlations between Fyn expression levels and clinical pathological features were assessed. We further detected the effects of Fyn on the proliferation, apoptosis, migration, and invasion of the pancreatic cancer cells through colony formation assay, flow cytometry (FCM) assay, wound healing assay, and transwell assay, respectively. The potential effects of Fyn on tumor growth were assessed using an animal model. We demonstrated the possible involvement of Fyn in the progression of pancreatic cancer. We found that Fyn was upregulated in human pancreatic cancer tissues and cells, and we analyzed the correlations between Fyn expression and the clinicopathological features, including metastasis staging (p=0.010*) and tumor size (p=0.025*) of patients with pancreatic cancer. Our data further confirmed that Fyn affects cell proliferation, apoptosis, migration, and invasion of pancreatic cancer cells via the phosphorylation of GluN2b and regulation of AKT signaling pathway. We also demonstrated that Fyn promoted tumor growth of pancreatic cancer cells in vivo. We investigated the potential involvement of Fyn in the progression of pancreatic cancer, and therefore indicated Fyn as a possible therapeutic target for pancreatic cancer.