{"title":"Deacetylation by SIRT6 increases the stability of GILZ to suppress NSCLC cell migration and invasion","authors":"","doi":"10.1016/j.cellsig.2024.111414","DOIUrl":null,"url":null,"abstract":"<div><p>Glucocorticoid-induced leucine zipper (GILZ) plays a role in cancer cell proliferation in several tumor types. However, in our present study, GILZ was demonstrated to be a metastasis regulator but not a proliferation regulator in non-small cell lung cancer (NSCLC). The overexpression of GILZ had no significant effect on the proliferation of NSCLC cells but inhibited their metastasis by targeting the epithelial-mesenchymal transition pathway. The deacetylase SIRT6, a key regulator of protein stability, can enhance the stability of the GILZ protein by mediating its deacetylation, which prevents ubiquitination and degradation. This process ultimately enhances the inhibitory effect of GILZ on the migration and invasion of NSCLC cells. Thus, GILZ may be a promising new therapeutic target for tumor metastasis.</p></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":null,"pages":null},"PeriodicalIF":4.4000,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular signalling","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0898656824003826","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Glucocorticoid-induced leucine zipper (GILZ) plays a role in cancer cell proliferation in several tumor types. However, in our present study, GILZ was demonstrated to be a metastasis regulator but not a proliferation regulator in non-small cell lung cancer (NSCLC). The overexpression of GILZ had no significant effect on the proliferation of NSCLC cells but inhibited their metastasis by targeting the epithelial-mesenchymal transition pathway. The deacetylase SIRT6, a key regulator of protein stability, can enhance the stability of the GILZ protein by mediating its deacetylation, which prevents ubiquitination and degradation. This process ultimately enhances the inhibitory effect of GILZ on the migration and invasion of NSCLC cells. Thus, GILZ may be a promising new therapeutic target for tumor metastasis.
期刊介绍:
Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo.
Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.