ArticleCell death & disease2020
Consequences of Zmat3 loss in c-MYC- and mutant KRAS-driven tumorigenesis.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- p53 Drives Lung Cancer Regression through a TSC2/TFEB-dependent Senescence Program.Cancer discovery · 2026Article
- The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024Article
- Upregulation of ZMAT3 is Associated with the Poor Prognosis of Breast Cancer.International journal of general medicine · 2024Article
- Unveiling the role of TGF-β signaling pathway in breast cancer prognosis and immunotherapy.Frontiers in oncology · 2024Article
- Nutlin-3 suppresses tumorigenesis and progression of oral squamous cell carcinoma and enhances chemosensitivity to cisplatin.Cytotechnology · 2023Article
- Review
- Of the many cellular responses activated by TP53, which ones are critical for tumour suppression?Cell death and differentiation · 2022Review
- miR-370 is better than miR-375 as a non-invasive diagnostic biomarker for pediatric acute myeloid leukemia patients.Cancer biomarkers : section A of Disease markers · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TP53 is a critical tumor suppressor that is mutated in approximately 50% of human cancers. Unveiling the downstream target genes of TP53 that fulfill its tumor suppressor function is an area of intense investigation. Zmat3 (also known as Wig-1 or PAG608) is one such downstream target of p53, whose loss in hemopoietic stem cells lacking the apoptosis and cell cycle regulators, Puma and p21, respectively, promotes the development of leukemia. The function of Zmat3 in tumorigenesis however remains unclear. Here, to investigate which oncogenic drivers co-operate with Zmat3 loss to promote neoplastic transformation, we utilized Zmat3 knockout mice in models of c-MYC-driven lymphomagenesis and Kras
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