ArticleCell death and differentiation2015
L-GILZ binds p53 and MDM2 and suppresses tumor growth through p53 activation in human cancer cells.
Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Isomucronulatol attenuates liver aging by inhibiting GSK-3β acetylation and promoting β-catenin accumulation.Journal of natural medicines · 2026Article
- Article
- Novel Insights into TSC22D Family Genes in Metabolic Diseases and Cancer.Biomolecules · 2026Review
- Glucocorticoids Downregulate PD-L1 in Glioblastoma Cells via GILZ-Mediated ERK Inhibition.Biomedicines · 2025Article
- L-GILZ is essential for cardiac function and protects against pressure overload-induced hypertrophy and dysfunction in mice.Asian heart journal · 2025Article
- Identification and Validation of a New Functional GeneStem cells international · 2025Article
- High expression of L-GILZ transcript variant 1 (GILZ TV 1) is associated with increased 30-day sepsis mortality, and a high expression ratio possibly contraindicates hydrocortisone administration.Critical care (London, England) · 2024Article
- Article
- Expression profiles of glucocorticoid-inducible proteins in human papilloma virus-related oropharyngeal squamous cell carcinoma.Frontiers in oral health · 2023Article
- Review
- P21 is not a prognostic marker for rectal cancer - five-year follow up study of rectal cancer in stages I-IV.Contemporary oncology (Poznan, Poland) · 2020Article
- β-Arrestin-1 inhibits glucocorticoid receptor turnover and alters glucocorticoid signaling.The Journal of biological chemistry · 2019Article
- A dual role for glucocorticoid-induced leucine zipper in glucocorticoid function: tumor growth promotion or suppression?Cell death & disease · 2018Review
- Genomic dissection of enhancers uncovers principles of combinatorial regulation and cell type-specific wiring of enhancer-promoter contacts.Nucleic acids research · 2018Article
- Long glucocorticoid-induced leucine zipper regulates human thyroid cancer cell proliferation.Cell death & disease · 2018Article
- Mechanistic Multi-Tissue Modeling of Glucocorticoid-Induced Leucine Zipper Regulation: Integrating Circadian Gene Expression with Receptor-Mediated Corticosteroid Pharmacodynamics.The Journal of pharmacology and experimental therapeutics · 2017Article
- Article
- Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- A focused Real Time PCR strategy to determine GILZ expression in mouse tissues.Results in immunology · 2015Article
- The novel partnership of L-GILZ and p53: a new affair in cancer?Molecular & cellular oncologyArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor p53 regulates the expression of genes crucial for biological processes such as cell proliferation, metabolism, cell repair, senescence and apoptosis. Activation of p53 also suppresses neoplastic transformations, thereby inhibiting the growth of mutated and/or damaged cells. p53-binding proteins, such as mouse double minute 2 homolog (MDM2), inhibit p53 activation and thus regulate p53-mediated stress responses. Here, we found that long glucocorticoid-induced leucine zipper (L-GILZ), a recently identified isoform of GILZ, activates p53 and that the overexpression of L-GILZ in p53(+/+) HCT116 human colorectal carcinoma cells suppresses the growth of xenografts in mice. In the presence of both p53 and MDM2, L-GILZ binds preferentially to MDM2 and interferes with p53/MDM2 complex formation, making p53 available for downstream gene activation. Consistent with this finding, L-GILZ induced p21 and p53 upregulated modulator of apoptosis (PUMA) expression only in p53(+/+) cells, while L-GILZ silencing reversed the anti-proliferative activity of dexamethasone as well as expression of p53, p21 and PUMA. Furthermore, L-GILZ stabilizes p53 proteins by decreasing p53 ubiquitination and increasing MDM2 ubiquitination. These findings reveal L-GILZ as a regulator of p53 and a candidate for new therapeutic anti-cancer strategies for tumors associated with p53 deregulation.
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