Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress

Amundson, Sally A.; Myers, Timothy G.; Fornace, Albert J.

doi:10.1038/sj.onc.1202576

Cited by 384 publications

(280 citation statements)

References 121 publications

(144 reference statements)

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“…These include the Rb and p53 proteins which are targeted by the viral E7 and E6 genes respectively (Dyson et al, 1989;Werness et al, 1990). The p53 tumour suppressor protein plays a pivotal role in cellular responses to stress factors such as DNA damage or hypoxia, principally through an induction of either cell cycle arrest or apoptosis (reviewed in Amundsen et al, 1998). An important mediator of the G1 arrest is the p21/WAF1 protein, a cdk inhibitor which is induced by transcriptional activation by activated p53 (El-Deiry et al, 1993;Petrocelli et al, 1996).…”

mentioning

confidence: 99%

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

2000

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In addition to their role in anogenital cancer, human papillomaviruses (HPVs) are also involved in the development of a range of cutaneous lesions. HPV types 5 and 8 are associated with the development of skin cancers in individuals with Epidermodysplasia verruciformis (EV). A broad spectrum of HPV types are also commonly found in non-melanoma skin cancers in immunocompromised individuals, such as organ transplant recipients. The skin cancers in EV and immunocompromised patients occur predominantly at body sites exposed to ultra violet (UV) radiation, pointing to a key role for UV in their development. Here we show that the E6 protein from a range of cutaneous HPV types e ectively inhibits apoptosis in response to UV damage. This occurs in both p53 null and wild type cells and does not require p53 degradation. Oncogene (2000) 19, 592 ± 598.

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mentioning

confidence: 99%

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

2000

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“…Since the pattern of cellular response to ST1926 involving p53 and drug-induced cell cycle arrest at G1 and S phases were reminiscent of the cellular response to DNA-damaging agents, 12 we investigated the effects of the drug on DNA integrity by the alkaline elution technique. Following 6 h exposure to drug concentrations in a range between the IC 50 and the IC 90 , the two cell lines exhibited a comparable extent of single-strand DNA breaks ( Figure 6).…”

Section: Dna Damagementioning

confidence: 99%

Induction of apoptosis and stress response in ovarian carcinoma cell lines treated with ST1926, an atypical retinoid

et al. 2003

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To understand the molecular mechanisms mediating apoptosis induction by a novel atypical retinoid, ST1926, the cellular response to drug treatment was investigated in IGROV-1 ovarian carcinoma cells carrying wild-type p53 and a cisplatin-resistant p53 mutant subline (IGROV-1/Pt1). Despite a similar extent of drug-induced DNA strand breaks, the level of apoptosis was substantially higher in p53 wild-type cells. p53 activation and early upregulation of p53-target genes were consistent with p53-dependent apoptosis in IGROV-1 cells. Stress-activated protein kinases were activated in both cell lines in response to ST1926. This event and activation of AP-1 were more pronounced in IGROV-1/Pt1 cells, in which the modulation of DNA repair-associated genes suggests an increased ability to repair DNA damage. Inhibition of JNK or p38 stimulated ST1926-induced apoptosis only in IGROV-1 cells, whereas inhibition of ERKs enhanced apoptosis in both the cell lines. Such a pattern of cellular response and modulation of genes implicated in DNA damage response supports that the genotoxic stress is a critical event mediating drug-induced apoptosis. The results are consistent with apoptosis induction through p53-dependent andindependent pathways, regulated by MAP kinases, which likely play a protective role.

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“…Activation of the p53 protein is observed following stress situations, such as DNA damage (Levine, 1997), oxidative stress (Renzing et al, 1996), microtubule disrupting agents (Jimenez et al, 1999), and hypoxia (Graeber et al, 1996). Elevated p53 activity leads to cell cycle arrest or apoptosis, depending on the cell type and the intensity of the stimulus (Amundson et al, 1998;Levine, 1997). Cell cycle arrest following p53 activation may occur at the G1/S or at the G2/M check points (Levine, 1997).…”

Section: Introductionmentioning

confidence: 99%

Isolation and characterization of sixteen novel p53 response genes

Kostic

Shaw

2000

Oncogene

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Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress

Cited by 384 publications

References 121 publications

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

Induction of apoptosis and stress response in ovarian carcinoma cell lines treated with ST1926, an atypical retinoid

Isolation and characterization of sixteen novel p53 response genes

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