| Literature DB >> 34845376 |
Mengjie Li1,2,3, Xianping Rao1,2,3, Yun Cui1,2,3, Lu Zhang1,2,3, Xiang Li1,2,3, Boya Wang3,4, Yijun Zheng1,2,5, Lisong Teng2,5, Tianhua Zhou6,7,8,9, Wei Zhuo10,11,12.
Abstract
DGC is a particular aggressive malignancy with poor prognosis. Recent omics studies characterized DGC with CDH1/E-cadherin loss and EMT-signatures. However, the underlying mechanisms for maintaining the aggressive behavior and molecular features of DGC remain unclear. Here, we find that intermediate filaments KRT17 is significantly lower in DGC tissues than that in intestinal gastric cancer tissues and associated with poor prognosis of DGC. We demonstrate that downregulation of KRT17 induces E-cadherin loss, EMT changes, and metastasis behaviors of GC cells. Mechanistically, the loss of intermediate filaments KRT17 induces reorganization of cytoskeleton, further activates YAP signaling, and increases IL6 expression, which contributes to the enhanced metastasis ability of GC cells. Together, these results indicate that KRT17/YAP/IL6 axis contributes to maintaining E-cadherin loss, EMT feature, and metastasis of DGC, providing a new insight into the role of aberrant intermediate filaments in DGC malignancy.Entities:
Mesh：
Year: 2021 PMID： 34845376 DOI： 10.1038/s41388-021-02119-3
Source DB: PubMed Journal: Oncogene ISSN： 0950-9232 Impact factor: 9.867