肿瘤的发展依赖于癌干细胞的干细胞特性，这是由环境信号调控的。以往的研究表明，Zyxin能够抑制胚胎干细胞状态的基因表达。本研究通过Western blot法分析了73例不同临床分期的胃癌患者癌组织和癌旁组织中Zyxin蛋白的表达水平。我们发现胃癌组织中Zyxin的相对表达水平（癌组织/癌旁组织）在晚期临床分期中明显下调。Zyxin的过表达抑制了胃癌细胞的干细胞特性和上皮间质转化（EMT）过程。Zyxin还抑制了癌细胞的增殖、迁移和侵袭，但增加了对药物的敏感性。在MKN45细胞中过表达Zyxin抑制了裸鼠中的肿瘤生长。我们发现Zyxin与SIRT1之间的相互作用导致了SIRT1的上调，降低了组蛋白H3 K9和K23的乙酰化水平，减少了SNAI 1/2的转录水平，抑制了EMT过程。本研究证明了Zyxin通过抑制癌干细胞的干细胞性和EMT来负向调控胃癌的进展。我们的发现为胃癌的发病机制提供了新的线索。本文照本发表于2023年由四川国际医学交流推广协会（SCIMEA）和John Wiley & Sons Australia, Ltd.出版的《医通通讯》杂志。

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.© 2023 The Authors. MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.