Zyxin Inhibits the Epithelial-Mesenchymal Transition Process in Gastric Cancer by Upregulating SIRT1
Publication Date
10-1-2023
Journal
MedComm
Abstract
Tumor development relies on the stemness of cancer stem cells, which is regulated by environmental cues. Previous studies have shown that zyxin can inhibit the expression of genes for embryonic stem cell status. In the present study, the expression levels of zyxin protein in cancer tissues and adjacent noncancerous tissues from 73 gastric cancer patients with different clinical stages were analyzed by Western blot. We showed that the relative expression levels of zyxin in gastric cancer tissues (cancer tissues/adjacent tissues) were significantly downregulated in advanced clinical stages. Overexpression of zyxin inhibited the stemness and epithelial-mesenchymal transition (EMT) processes in gastric cancer cells. Zyxin also inhibited the proliferation, migration, and invasion but increased the sensitivity of cancer cells to drugs. Overexpression of zyxin in MKN45 cells inhibited tumor growth in nude mice. We show that the interactions between zyxin and SIRT1 led to the upregulation of SIRT1, reduced acetylation levels of histone H3 K9 and K23, decreased transcription levels of SNAI 1/2, and inhibition of the EMT process. This study demonstrated that zyxin negatively regulates the progression of gastric cancer by inhibiting the stemness of cancer stem cells and EMT. Our findings shed new light on the pathogenesis of gastric cancer.
Keywords
acetylation, EMT;SIRT1, gastric cancer, zyxin
Included in
Bioinformatics Commons, Biomedical Informatics Commons, Gastroenterology Commons, Hepatology Commons, Internal Medicine Commons, Medical Sciences Commons, Oncology Commons
Comments
Supplementary Materials
PMID: 37667739