The Contrived Mutant p53 Oncogene – Beyond Loss of Functions
نویسندگان
چکیده
منابع مشابه
The Contrived Mutant p53 Oncogene – Beyond Loss of Functions
Mutations in p53 are almost synonymous with cancer - be it susceptibility to the disease or response to treatment - and therefore, are a critical determinant of overall survival. As most of these mutations occur in the DNA-binding domain of p53, many of the clinical correlations with mutant p53 have been initially relegated to the loss of its transcription-dependent activities as a tumor suppre...
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P53 mutation plays a pivotal role in tumorigenesis of endometrial cancer (EC), here we report that the gain-of-function mutant p53-R248Q targets the proteasome activator REGγ to promote EC progression. Increased p53 expression significantly correlated with high pathological grade and lymph node metastasis in EC specimens. Manipulation of p53-R248Q in EC cells caused coincident changes in REGγ e...
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Oncogene-mediated cellular transformation is a multistep process involving activation of growth-promoting pathways as well as inactivation of tumor suppressors. We recently found that ISGylation of the p53 tumor suppressor is an important novel mechanism to control its stability. Here we identified that Isg15-dependent regulation of p53 can be enhanced by different oncogenes. We further show th...
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Breast cancer is the most frequent invasive tumor diagnosed in women, causing over 400 000 deaths yearly worldwide. Like other tumors, it is a disease with a complex, heterogeneous genetic and biochemical background. No single genomic or metabolic condition can be regarded as decisive for its formation and progression. However, a few key players can be pointed out and among them is the TP53 tum...
متن کاملMutant p53 exerts oncogenic functions by modulating cancer cell metabolism
The metabolic function of p53 is important for its oncosuppressive function. Mutant p53 (mutp53) with gain of oncogenic function can regulate cell metabolism. Our recent study revealed a novel transcription-independent mechanism for a gain-of-function mutp53 that directly inhibits activation of adenosine monophosphate-activated protein kinase (AMPK) to promote cancer cell metabolism.
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ژورنال
عنوان ژورنال: Frontiers in Oncology
سال: 2015
ISSN: 2234-943X
DOI: 10.3389/fonc.2015.00276