2012
Abstract: The P53 gene and it product p53 protein is the most studied tumor suppressor, which was considered as oncogene for two decades until 1990. More than 60 thousand papers on the topic of p53 has been abstracted in Pubmed. What yet could be discovered about its role in cell death, growth arrest and apoptosis, as well as a mediator of the therapeutic effect of anticancer drugs. Still during recent few years even more amazing discoveries have been done. Here we review such topics as suppression of epigenetic silenci…
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Cited by 16 publications
(10 citation statements)
References 146 publications
(80 reference statements)
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“…It is well established that p53 regulates cellular behavior of cancer cells by transcriptional regulation of specific genes or signaling pathways implicated in those activities (28)(29)(30)(31)(32)(33)(34). However, our results showed that BRD7 could induce tumor suppressive effects in either SKOV3 (p53 null) or A2780 (p53 wild type) cells.…”
Section: Discussioncontrasting
confidence: 72%
“…[11][12][13][14][15] It is involved in several biological processes, such as cell death, [16][17][18][19] differentiation, [20][21][22] neuronal stem cell maintenance, [23][24][25][26] the amino acid Glutamine is converted into Glutamate by a deamidation reaction catalyzed by the enzyme Glutaminase (GLS). two isoforms of this enzyme have been described, and the GLS2 isoform is regulated by the tumor suppressor gene p53.…”
Section: Introductionmentioning
confidence: 99%
“…Indeed, aging is not just cell cycle arrest. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] In analogy, although cell cycle progression is important in carcinogenesis, we do not define cancer as cell cycle progression. For one, intestinal and bone marrow progenitor cells proliferate faster than tumor cells.…”
Section: Introductionmentioning
confidence: 99%
“…Partially reduced activity of the gene mth (short for "methuselah") extends the average lifespan of Drosophila melanogaster (the fruit fly) by about 35 %, [36] and mutations in its daf-2 gene also increases longev-ity [30]. Inhibition of the TOR (target of rapamycin) metabolic pathway decelerates premature senescence in cells whose cycle is blocked and can extend lifespan in C. elegans, Drosophila, and mice [9,37].…”
Section: Longevity and Genesmentioning
confidence: 99%
“…By causing arrest of the cell cycle when it detects DNA damage or other issues within a cell, p53 may either indirectly or directly contribute to the cell becoming senescent [43,87,92]. The p53 gene can in some cases repair cellular DNA and in others help induce senescence, apoptosis (induction of cell death if the cell is beyond repair), or quiescence (a temporary state of reduced activity and cell division arrest short of permanent senescence) in a damaged cell [37,52,87,[100][101][102][103].…”
Section: The Hayflick and Other Limitsmentioning
confidence: 99%
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