Coexpression of p21<sup>Waf1/Cip1</sup>
 and p53 in sun-exposed normal epidermis, but not in neoplastic epidermis

Inohara, Shinichi; Kitagawa, Keiko; Kitano, Yukio

doi:10.1046/j.1365-2133.1996.d01-1068.x

Cited by 9 publications

(9 citation statements)

References 11 publications

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“…Coexpression of p53 and p21 was seen in only 2 cases in our material. This con®rms reports from other studies (28,29) and probably indicates the defective action of a mutated p53 and p21 induction by a p53-independent pathway. Colocalization is the rule when the physiological p53/p21 response to UV radiation is studied (26,43).…”

Section: Discussionsupporting

confidence: 91%

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Expression of p21 WAF1/CIP1 , p53, bcl-2 and Ki-67 in Venous Leg Ulcers with and without Squamous Cell Carcinoma

Baldursson

Syrjänen²,

Beitner³

2000

Acta Dermato-Venereologica

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In order to gain understanding of the cellular mechanisms of malignant transformation in chronic venous leg ulcers, we analysed by immunohistochemistry the presence of p21, p53, bcl-2 and Ki-67 in ulcers with and without squamous cell carcinoma. The material consisted of 41 archived histopathological samples from 33 patients with chronic venous leg ulcers and 28 samples from 21 patients suffering from squamous cell carcinoma in chronic venous leg ulcers. All samples derived from the chronic ulcers were negative for p53, p21 and bcl-2. Cells positive for Ki-67 were seen in certain ulcer areas. In the cancers, 14 samples showed immunopositivity for p53 and 22 samples were positive for p21, with expression mainly in the suprabasal layer. Expression of p21 seemed independent of p53. None of the samples was bcl-2-positive. Ki-67 was positive with basal expression in 16/28 of the tumour samples, 15 of which also expressed p21. There was no perilesional p53 or p21 activity in the cancer samples. The results regarding perilesional expression are different from those reported in UV-induced squamous cell carcinomas and probably reflect a different carcinogen.

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Section: Discussionsupporting

confidence: 91%

“…The existence of upstream inducers of p21 other than p53 is reported in a number of papers (26,32,33). Expression of p21 in SCC is usually independent of p53 (28,29), even in non-skin SCCs (34,35).…”

mentioning

confidence: 98%

Expression of p21 WAF1/CIP1 , p53, bcl-2 and Ki-67 in Venous Leg Ulcers with and without Squamous Cell Carcinoma

Baldursson

Syrjänen²,

Beitner³

2000

Acta Dermato-Venereologica

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“…13 is supported by the rapid (Ͼ50% within 2 h) decrease in the proportion of keratinocytes engaged in DNA synthesis after irradiation with UVB (unpublished data). It is thought that the major mediator of cell cycle arrest in UVirradiated cells is the p53 tumor suppressor (29). Surprisingly, we found that UVB irradiation of HEKn (p53-proficient cells [ Fig.…”

mentioning

confidence: 39%

The UV (Ribotoxic) Stress Response of Human Keratinocytes Involves the Unexpected Uncoupling of the Ras-Extracellular Signal-Regulated Kinase Signaling Cascade from the Activated Epidermal Growth Factor Receptor

Iordanov

Choi

Ryabinina

et al. 2002

Molecular and Cellular Biology

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In mammals, UVB radiation is of biological relevance primarily for the cells of the epidermis. We report here the existence of a UVB response that is specific for proliferating human epidermal keratinocytes. Unlike other cell types that also display a UVB response, keratinocytes respond to UVB irradiation with a transient but potent downregulation of the Ras-extracellular signal-regulated kinase (ERK) signaling cascade. The downregulation of ERK precedes a profound decrease in the steady-state levels of cyclin D1, a mediator of the proliferative action of ERK. Keratinocytes exhibit high constitutive activity of the Ras-ERK signaling cascade even in culture medium lacking supplemental growth factors. The increased activity of Ras and phosphorylation of ERK in these cells are maintained by the autocrine production of secreted molecules that activate the epidermal growth factor receptor (EGFR). Irradiation of keratinocytes increases the phosphorylation of EGFR on tyrosine residues Y845, Y992, Y1045, Y1068, Y1086, Y1148, and Y1173 above the basal levels and leads to the increased recruitment of the adaptor proteins Grb2 and ShcA and of a p55 form of the regulatory subunit of the phosphatidylinositide 3-kinase to the UVB-activated EGFR. Paradoxically, however, UVB causes, at the same time, the inactivation of Ras and a subsequent dephosphorylation of ERK. By contrast, the signaling pathway leading from the activated EGFR to the phosphorylation of PKB/Akt1 is potentiated by UVB. The UVB response of keratinocytes appeared to be a manifestation of the more general ribotoxic stress response inasmuch as the transduction of the UVB-generated inhibitory signal to Ras and ERK required the presence of active ribosomes at the time of irradiation.

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“…In epidermis, p21 Cip1 levels increase in response to cell stress, and it is heterogeneously expressed in skin cancer cells (14,(21)(22)(23)(24). Of particular interest is the fact that p21…”

Section: Sulforaphane (Sfn)mentioning

confidence: 99%

Sulforaphane Induction of p21Cip1 Cyclin-dependent Kinase Inhibitor Expression Requires p53 and Sp1 Transcription Factors and Is p53-dependent

Chew

Adhikary

Wilson

et al. 2012

Journal of Biological Chemistry

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Background: Sulforaphane is an important cancer preventative in skin cancer. Results: SFN induces p21Cip1 via a p53-dependent mechanism that involves p53 stabilization. Conclusion: p21Cip1 expression is differentially regulated in normal keratinocytes versus cancer cells. Significance: SFN treatment will slow proliferation of normal epidermal keratinocytes but will cause resident cancer cell apoptosis.

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Coexpression of p21^Waf1/Cip1 and p53 in sun-exposed normal epidermis, but not in neoplastic epidermis

Cited by 9 publications

References 11 publications

Expression of p21 WAF1/CIP1 , p53, bcl-2 and Ki-67 in Venous Leg Ulcers with and without Squamous Cell Carcinoma

Expression of p21 WAF1/CIP1 , p53, bcl-2 and Ki-67 in Venous Leg Ulcers with and without Squamous Cell Carcinoma

The UV (Ribotoxic) Stress Response of Human Keratinocytes Involves the Unexpected Uncoupling of the Ras-Extracellular Signal-Regulated Kinase Signaling Cascade from the Activated Epidermal Growth Factor Receptor

Sulforaphane Induction of p21Cip1 Cyclin-dependent Kinase Inhibitor Expression Requires p53 and Sp1 Transcription Factors and Is p53-dependent

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Coexpression of p21Waf1/Cip1 and p53 in sun-exposed normal epidermis, but not in neoplastic epidermis

Cited by 9 publications

References 11 publications

Expression of p21 WAF1/CIP1 , p53, bcl-2 and Ki-67 in Venous Leg Ulcers with and without Squamous Cell Carcinoma

Expression of p21 WAF1/CIP1 , p53, bcl-2 and Ki-67 in Venous Leg Ulcers with and without Squamous Cell Carcinoma

The UV (Ribotoxic) Stress Response of Human Keratinocytes Involves the Unexpected Uncoupling of the Ras-Extracellular Signal-Regulated Kinase Signaling Cascade from the Activated Epidermal Growth Factor Receptor

Sulforaphane Induction of p21Cip1 Cyclin-dependent Kinase Inhibitor Expression Requires p53 and Sp1 Transcription Factors and Is p53-dependent

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Coexpression of p21^Waf1/Cip1 and p53 in sun-exposed normal epidermis, but not in neoplastic epidermis