![]() (B) Cell expansion assay was performed over 3 days to analyze proliferation in stable H1299 cells. Densitometry analyses of the bands are indicated over β-actin. β-Actin was used as a loading control ( n = 4). (A) Western blots showing the expression levels of p53 and p21 (a transcriptional target of wt p53) in H1299 control (CV) and stable expression of indicated mutant p53 proteins. Our investigation highlights the diversity of different p53 mutants in terms of their effect on metabolism, which might provide a foundation for the development of more effective targeted pharmacological approaches toward variants of mutant p53.ĮMT OxPhos cancer glycolysis metabolism mutant p53.Ĭopyright © 2017 American Society for Microbiology.Įffect of mutant p53 proteins on glycolysis. In this study, we have metabolically profiled several individual frequently occurring p53 mutants in cancers, focusing on glycolytic and mitochondrial oxidative phosphorylation pathways. Accordingly, the effect of different mutant p53 proteins on cancer cell metabolism is largely unknown. There is a strong rationale that the GOF activities, including alterations in cellular metabolism, might vary between the different p53 mutants. Recently, mutant p53 proteins have been shown to mediate metabolic changes as a novel GOF to promote tumor development. Unlike other tumor suppressors that are frequently deleted or acquire loss-of-function mutations, the majority of TP53 mutations in tumors are missense substitutions, which lead to the expression of full-length mutant proteins that accumulate in cancer cells and may confer unique gain-of-function (GOF) activities to promote tumorigenic events. TP53 is one of the most commonly mutated genes in human cancers. ![]()
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