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Expression of the novel tumour suppressor p33(ING1)is independent of p53.

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Affiliations

  • 1. Department of Medicine, Division of Dermatology, University of British Columbia, Vancouver, British Columbia, V6H 3Z6, Canada.
      Authors
    • Cheung KJ Jr 1
    (1 author)

British Journal of Cancer, 01 Dec 2000, 83(11):1468-1472
https://doi.org/10.1054/bjoc.2000.1464 PMID: 11076655 PMCID: PMC2363422

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Abstract 

A recently cloned tumour suppressor candidate, p33ING1, has been shown in vitro to collaborate with p53 to execute growth arrest and apoptosis. However, it is unclear as to how the expression of ING1 is regulated in normal and stress conditions. Using a p53-knockout mouse model, we investigated if the expression of ING1 was dependent on p53. We found that there was no difference in ING1 mRNA and protein levels between p53+/+ and p53-/- murine organs. In addition, when normal human epithelial keratinocytes (NHEK) and a keratinocyte cell line, HaCaT, which lacks wild-type p53 function, were exposed to UVB irradiation, the expression levels of ING1 were elevated in both NHEK and HaCaT cells. It is interesting, however, that UVB irradiation did not induce ING1 expression in dermal fibroblasts isolated from p53+/+ and p53-/- mice. Based on our findings, we therefore conclude that the expression of ING1 is independent of p53 status. UV induction of ING1 in keratinocytes suggests that ING1 may play a role in cellular stress response and skin carcinogenesis.

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Logo of brjcancerBJC HomepageBJC Advance online publicationBJC Current IssueSubmitting an article to BJCWeb feeds
Br J Cancer. 2000 Dec; 83(11): 1468–1472.
Published online 2000 Nov 22. https://doi.org/10.1054/bjoc.2000.1464
PMCID: PMC2363422
PMID: 11076655

Expression of the novel tumour suppressor p33ING1 is independent of p53

K-J J Cheung, Jr,1 J A Bush,1 W Jia,2 and G Li1
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Abstract

A recently cloned tumour suppressor candidate, p33ING1, has been shown in vitro to collaborate with p53 to execute growth arrest and apoptosis. However, it is unclear as to how the expression of ING1 is regulated in normal and stress conditions. Using a p53-knockout mouse model, we investigated if the expression of ING1 was dependent on p53. We found that there was no difference in ING1 mRNA and protein levels between p53+/+ and p53–/– murine organs. In addition, when normal human epithelial keratinocytes (NHEK) and a keratinocyte cell line, HaCaT, which lacks wild-type p53 function, were exposed to UVB irradiation, the expression levels of ING1 were elevated in both NHEK and HaCaT cells. It is interesting, however, that UVB irradiation did not induce ING1 expression in dermal fibroblasts isolated from p53+/+ and p53–/– mice. Based on our findings, we therefore conclude that the expression of ING1 is independent of p53 status. UV induction of ING1 in keratinocytes suggests that ING1 may play a role in cellular stress response and skin carcinogenesis. © 2000 Cancer Research Campaign http://www.bjcancer.com

Keywords: p33ING1, p53, in vivo expression, tumour suppressor gene, UV irradiation
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Selected References
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