p21 (CDKN1A) is a Negative Regulator of p53 Stability

Broude, Eugenia V.; Demidenko, Zoya N.; Vivo, Claire; Swift, Mari E.; Davis, Brian M.; Blagosklonny, Mikhail V.; Roninson, Igor B.

doi:10.4161/cc.6.12.4313

Cited by 63 publications

(46 citation statements)

References 33 publications

(60 reference statements)

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“…It has been widely observed that deletion of CDKN1A (encodes p21) in HCT116 cells leads to increased stabilization and accumulation of p53 (39,40). We confirmed this increase of p53 protein in p21 Ϫ/Ϫ cells compared with HCT116 cells (Fig.…”

Section: Modulation Of P53 or Treatment With 5aza-dc Leads To Local Csupporting

confidence: 78%

Local Depletion of DNA Methylation Identifies a Repressive p53 Regulatory Region in the NEK2 Promoter

Nabilsi

Ryder

Peraza-Penton

et al. 2013

Journal of Biological Chemistry

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Background: NEK2 is a mammalian kinase that promotes centrosome separation during the cell cycle. Results: Agents that demethylate the NEK2 promoter or induce DNA damage repress NEK2 expression in a p53-dependent manner. Conclusion: p53 represses NEK2 expression and protects its binding region from accumulating DNA methylation. Significance: Knowledge regarding novel mechanisms of NEK2 regulation may help inform clinical application of NEK2-based anticancer therapeutics.

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Section: Modulation Of P53 or Treatment With 5aza-dc Leads To Local Csupporting

confidence: 78%

Local Depletion of DNA Methylation Identifies a Repressive p53 Regulatory Region in the NEK2 Promoter

Nabilsi

Ryder

Peraza-Penton

et al. 2013

Journal of Biological Chemistry

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“…We did not observe a release from p21 WAF1 -mediated growth arrest upon drug-treatment, which may explain why cells did not enter mitosis and mitotic catastrophe [44]. Induction of p21 WAF1 in cells containing wild-type p53 may result in genetic destabilization [3,45]. However, the p21 WAF1 levels did not maintain growth arrest and senescence; tentatively because of the changes in other protein levels (Fig.…”

Section: Discussionmentioning

confidence: 74%

A nuclear budding mechanism in transiently arrested cells generates drug-sensitive and drug-resistant cells

Mansilla

Bataller

Portugal

2009

Biochemical Pharmacology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 and the meiosis-related Mos. The buds might be a mechanism for the segregation and elimination of redundant DNA, or for generating viable aneuploid cells with a potentially extended life span.

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“…On the other hand, previous reports have shown that p21 can negatively regulate p53 stability in different cell types in the context of a normal DNA damage response (34). In HT1080p21-9, neither p53 nor its targets genes, HDM2…”

Section: P21 Expression Can Induce Both Cell Cycle Arrest and Death Imentioning

confidence: 90%

Reactive Oxygen Species and Mitochondrial Sensitivity to Oxidative Stress Determine Induction of Cancer Cell Death by p21

Masgras

Carrera

Verdier

et al. 2012

Journal of Biological Chemistry

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Background: For unknown reasons, p21 expression induces different effects in cells, including arrest, death, and growth/ prosurvival signals. Results: Cancer cell lines respond with arrest or apoptosis to p21 expression depending on mitochondria sensitivity to oxidants. Conclusion: Cell-specific sensitivity to oxidative stress determines p21-induced cell death.Significance: This provides a rationale to find therapies that up-regulate p21 in cells that are more sensitive to oxidants to favor a death response.

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p21 (CDKN1A) is a Negative Regulator of p53 Stability

Cited by 63 publications

References 33 publications

Local Depletion of DNA Methylation Identifies a Repressive p53 Regulatory Region in the NEK2 Promoter

Local Depletion of DNA Methylation Identifies a Repressive p53 Regulatory Region in the NEK2 Promoter

A nuclear budding mechanism in transiently arrested cells generates drug-sensitive and drug-resistant cells

Reactive Oxygen Species and Mitochondrial Sensitivity to Oxidative Stress Determine Induction of Cancer Cell Death by p21

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