ArticleMolecular cancer2010
FATS is a transcriptional target of p53 and associated with antitumor activity.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Diagnostic and prognostic potential of cell-free RNAs in cerebrospinal fluid and plasma for brain tumors.NPJ precision oncology · 2025Article
- FATS inhibits the Wnt pathway and induces apoptosis through degradation of MYH9 and enhances sensitivity to paclitaxel in breast cancer.Cell death & disease · 2024Article
- Association study betweenFrontiers in oncology · 2023Article
- Gene losses may contribute to subterranean adaptations in naked mole-rat and blind mole-rat.BMC biology · 2022Article
- Loss of fragile site-associated tumor suppressor promotes antitumor immunity via macrophage polarization.Nature communications · 2021Article
- FATS regulates polyamine biosynthesis by promoting ODC degradation in an ERβ-dependent manner in non-small-cell lung cancer.Cell death & disease · 2020Article
- Article
- The value of FATS expression in predicting sensitivity to radiotherapy in breast cancer.Oncotarget · 2017Article
- A functional genetic variant in fragile-site gene FATS modulates the risk of breast cancer in triparous women.BMC cancer · 2015Article
- NKX3.1 Suppresses TMPRSS2-ERG Gene Rearrangement and Mediates Repair of Androgen Receptor-Induced DNA Damage.Cancer research · 2015Article
- FATS is an E2-independent ubiquitin ligase that stabilizes p53 and promotes its activation in response to DNA damage.Oncogene · 2014Article
- Melanocytes in the skin--comparative whole transcriptome analysis of main skin cell types.PloS one · 2014Article
- Common fragile sites: genomic hotspots of DNA damage and carcinogenesis.International journal of molecular sciences · 2012Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frequent mutations of p53 in human cancers exemplify its crucial role as a tumor suppressor transcription factor, and p21, a transcriptional target of p53, plays a central role in surveillance of cell-cycle checkpoints. Our previous study has shown that FATS stabilize p21 to preserve genome integrity. In this study we identified a novel transcript variant of FATS (GenBank: GQ499374) through screening a cDNA library from mouse testis, which uncovered the promoter region of mouse FATS. Mouse FATS was highly expressed in testis. The p53-responsive elements existed in proximal region of both mouse and human FATS promoters. Functional study indicated that the transcription of FATS gene was activated by p53, whereas such effect was abolished by site-directed mutagenesis in the p53-RE of FATS promoter. Furthermore, the expression of FATS increased upon DNA damage in a p53-dependent manner. FATS expression was silent or downregulated in human cancers, and overexpression of FATS suppressed tumorigenicity in vivo independently of p53. Our results reveal FATS as a p53-regulated gene to monitor genomic stability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.