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Regulation of the cell fate by DNA damage and hypoxia

World Journal of Medical Genetics 2013年第4期3卷 34-40页

作者： Ramkumar Rajendran Marija Krstic-Demonacos Constantinos Demonacos international Medical University Bukit JalilKuala Lumpur 57000Malaysia School of Environment and Life Sciences College of Science and TechnologyCockcroft BuildingUniversity of SalfordManchester M5 4WTUnited Kingdom Molecular Pharmacology and Cancer Biology Faculty of Medical and Human SciencesManchester Pharmacy SchoolUniversity of ManchesterManchester M139PTUnited Kingdom

in order to provide the means for the design of novel rational anti-cancer drug therapies research efforts are concentrated on unravelling the molecular circuits which induce programmed cell death and block proliferation of cancer *** therapeutic strategies are based on the understanding of the complexity of physiological functions such as differentiation,development,immune responses,cell-cycle arrest,DNA damage repair,apoptosis,autophagy,energy metabolism,and *** has become evident that this knowledge will provide the means to target the components of the pathways involved in these processes in a specific and selective manner thus paving the way for the development of effective and personalised anti-cancer *** is a crucial cellular process that regulates a multitude of physiological functions,which are essential in disease progression and cellular response to *** factors such as the p53 tumor suppressor and the hypoxia-inducible factor-α(HiF-α) are key players in carcinogenesis and cellular response to cancer *** of these transcription factors regulate gene expression of genes involved in cell death and proliferation,in some cases cooperating towards producing the same outcome and in some others mediating opposing *** is thus apparent that fine tuning of the activity of these transcription factors is essential to determine the cellular response to therapeutic regimens,in other words whether tumor cells will commit to apoptosis or evade engagement with the anti-proliferative effects of drugs leading to drug *** observations support the notion that the functional crosstalk between HiF-1α and p53 pathways and thus the fine tuning of their transcriptional activity is mediated by cofactors shared between the two transcription factors such as components of the p300 co-activator multiprotein *** particular,there is evidence to suggest that differential composition of the co-modula

关键词： Cancer Transcription Apoptosis inflammation Tumor energy metabolism Glyco lysis Oxidati ve phos phorylatio n p53 hypoxia-i nduci ble facto r p300/CBP associated factors

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