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Effects of ΔNp73β on Cisplatin Treatment in Colon Cancer Cells
University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
Linköping University.
Linköping University.
Linköping University.
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2012 (English)In: Molecular Carcinogenesis, ISSN 0899-1987, E-ISSN 1098-2744, Vol. 51, no 8, p. 628-635Article in journal (Refereed) Published
Abstract [en]

p73 can activate transcription of p53-responsive genes, thereby inhibiting cell growth. An alternative promoter in the TP73 gene gives rise to an N-terminally truncated isoform of p73, DNp73, which lacks the transactivation domain of the full length TAp73 protein. TAp73 is considered pro-apoptotic, and DNp73 anti-apoptotic. In this study, we overexpressed DNp73β in p53 wild type and p53 mutant colon cancer cell lines and further exposed the cells to cancer therapeutic drug cisplatin. The results showed that cisplatin decreased the protein expression levels of DNp73β in a dose-dependent manner, and both TAp73 and p53 were upregulated after cisplatin treatment. Further, clonogenic potential and cell viability were decreased, and apoptotic cells increased, in p53 mutant and in p53 wild type cells. Cellular viability was significantly higher in DNp73β-cells than mock-transfected cells. However, DNp73β overexpression did not affect the cellular susceptibility to cisplatin. In conclusion, the overexpression of DNp73β increases viability in p53 wild type and p53 mutant colon cancer cells, and cisplatin induces the degradation of DNp73β in a dose-dependent manner.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2012. Vol. 51, no 8, p. 628-635
Keywords [en]
cell death, HCT116 cells, HT29 cells, p73 protein, p53
National Category
Cancer and Oncology Cell and Molecular Biology
Research subject
Natural sciences
Identifiers
URN: urn:nbn:se:his:diva-5813DOI: 10.1002/mc.20835ISI: 000305962400004Scopus ID: 2-s2.0-84863477921OAI: oai:DiVA.org:his-5813DiVA, id: diva2:524383
Available from: 2012-05-02 Created: 2012-05-02 Last updated: 2021-08-03Bibliographically approved

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Lööf, JasmineZhang, Hong

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