p53 and DNA methylation suppress the TRAIN to cell death

Tavana, Omid; Gu, Wei

Hallmark to most cancers is the mutation or complete loss of function of the tumor-suppressor gene p53. p53 functions by transcriptionally activating or repressing putative downstream targets to elicit a network of tumor-suppressive functions—transient cell cycle arrest allowing for DNA repair and, upon irreparable damage, senescence or apoptosis. Recently, our group has shown that p53-meidated transactivation of metabolic targets can suppress tumorigenesis in the absence of both cell cycle arrest and apoptosis. Notably termed the “guardian of the genome,” many therapies have been targeted to reactivate p53 or the downstream targets to initiate apoptosis or cell cycle arrest in cells that have escaped these properties, yet in some instances, p53-proficient tumors have a worse response to therapy. An opposite and ever-attractive chemotherapeutic approach has been to selectively target attributes of p53-mutant and -deficient cells that are absent in p53 proficiency.


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Cell Cycle

More About This Work

Academic Units
Institute for Cancer Genetics
Published Here
July 11, 2013