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CD36 upregulates DEK transcription and promotes cell migration and invasion via GSK-3β/β-catenin-mediated epithelial-to-mesenchymal transition in gastric cancer

Jin Wang, Ti Wen, Zhi Li, Xiaofang Che, Libao Gong, Zihan Jiao, Xiujuan Qu, Yunpeng Liu

2020Aging44 citationsDOIOpen Access PDF

Abstract

= 0.030) in 79 Chinese GC patients. Basal CD36 expression levels correlated positively with migration, invasion, and expression of epithelial-to-mesenchymal transition (EMT) markers in GC cell lines, a relationship confirmed by knockdown and overexpression experiments. Importantly, analysis of gene expression changes in CD36-knockdown GC cells led us to identify the chromatin-associated protein DEK as a c-Myc target that mediates activation of the GSK-3β/β-catenin signaling pathway to trigger EMT. These findings further our understanding of the mechanisms governing metastatic dissemination of GC cells and suggest the therapeutic potential of strategies targeting CD36.

Topics & Concepts

Gene knockdownEpithelial–mesenchymal transitionCancer researchCD36MetastasisBiologyCancerCancer cellApoptosisReceptorGeneticsCancer, Lipids, and MetabolismPeroxisome Proliferator-Activated ReceptorsCholangiocarcinoma and Gallbladder Cancer Studies
CD36 upregulates DEK transcription and promotes cell migration and invasion via GSK-3β/β-catenin-mediated epithelial-to-mesenchymal transition in gastric cancer | Litcius