Fhit and Wwox loss-associated genome instability: A genome caretaker one-two punch
نویسندگان
چکیده
منابع مشابه
Initiation of Genome Instability and Preneoplastic Processes through Loss of Fhit Expression
Genomic instability drives tumorigenesis, but how it is initiated in sporadic neoplasias is unknown. In early preneoplasias, alterations at chromosome fragile sites arise due to DNA replication stress. A frequent, perhaps earliest, genetic alteration in preneoplasias is deletion within the fragile FRA3B/FHIT locus, leading to loss of Fhit protein expression. Because common chromosome fragile si...
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FHIT, located at FRA3B, is one of the most commonly deleted genes in human cancers, and loss of FHIT protein is one of the earliest events in cancer initiation. However, location of FHIT at a chromosomal fragile site, a locus prone to breakage and gap formation under even mild replication stress, has encouraged claims that FHIT loss is a passenger event in cancers. We summarize accumulated evid...
متن کاملThe one-two punch
The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARβ/δ and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARβ/δ. In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RARγ to induce the expression of hallmark markers of preadipocyte...
متن کاملWWOX guards genome stability by activating ATM
Common fragile sites (CFSs) tend to break upon replication stress and have been suggested to be "hot spots" for genomic instability. Recent evidence, however, implies that in the wake of DNA damage, WW domain-containing oxidoreductase (WWOX, the gene product of the FRA16D fragile site), associates with ataxia telangiectasia-mutated (ATM) and regulates its activation to maintain genomic integrity.
متن کاملFhit Deficiency-Induced Global Genome Instability Promotes Mutation and Clonal Expansion
Loss of Fhit expression, encoded at chromosome fragile site FRA3B, leads to increased replication stress, genome instability and accumulation of genetic alterations. We have proposed that Fhit is a genome 'caretaker' whose loss initiates genome instability in preneoplastic lesions. We have characterized allele copy number alterations and expression changes observed in Fhit-deficient cells in co...
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ژورنال
عنوان ژورنال: Advances in Biological Regulation
سال: 2017
ISSN: 2212-4926
DOI: 10.1016/j.jbior.2016.09.008