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Deacetylation by SIRT6 increases the stability of GILZ to suppress NSCLC cell migration and invasion. | LitMetric

Deacetylation by SIRT6 increases the stability of GILZ to suppress NSCLC cell migration and invasion.

Cell Signal

School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, PR China. Electronic address:

Published: December 2024

AI Article Synopsis

  • GILZ is a protein that helps control how cancer cells spread (metastasis) in certain types of cancer, especially non-small cell lung cancer (NSCLC).
  • In this study, scientists found that while GILZ doesn't stop cancer cells from growing, it does stop them from spreading to other parts of the body.
  • Another protein called SIRT6 helps keep GILZ stable so it can work better against cancer cell movement, making GILZ a potential target for new cancer treatments.

Article 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.

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Source
http://dx.doi.org/10.1016/j.cellsig.2024.111414DOI Listing

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