Abstract A39: The activation of {beta}1-integrin by type i collagen coupling with the Hedgehog pathway promotes the epithelial-mesenchymal transition in pancreatic cancer cells

In this study, we demonstrated that pancreatic cancer cells exhibited increased proliferation and decreased apoptosis in response to type I collagen. In addition, exposed to type I collagen, PDAC cells lost the expression of E-cadherin and increased expression of mesenchymal markers, including N-cadherin and vimentin, which was correlated with enhanced cell migration and invasiveness. Conversely, the knockdown of β1-integrin abolished the effects induced by type I collagen. Further investigation revealed that type I collagen activates β1-integrin accompanied with significant up-regulation of Gli-1. siRNA specific to Gli-1 reversed the effects of type I collagen on PDAC invasion and epithelial-mesenchymal transition (EMT). These results suggest that there is cross-talk between the β1-integrin signaling pathway and the Hedgehog (HH) pathway in pancreatic cancer and the abnormal activation of the HH pathway plays a key role in the type I collagen-induced effects on pancreatic cancer. Therefore, our findings may have potential significance for the development of new therapeutic strategies to treat this highly aggressive malignancy.Citation Format: Wanxing Duan, Qingyong Ma, Jiguang Ma, Qinhong Xu, Jianjun Lei, Erxi Wu. The activation of β1-integrin by type i collagen coupling with the Hedgehog pathway promotes the epithelial-mesenchymal transition in pancreatic cancer cells. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Resear...
Source: Cancer Research - Category: Cancer & Oncology Authors: Tags: Development Source Type: research