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Effects of Delta Np73 beta on cisplatin treatment in colon cancer cells
University of Skovde, Sweden .
Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
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2012 (English)In: Molecular Carcinogenesis, ISSN 0899-1987, E-ISSN 1098-2744, Vol. 51, no 8, 628-635 p.Article 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, Delta Np73, which lacks the transactivation domain of the full length TAp73 protein. TAp73 is considered pro-apoptotic, and Delta Np73 anti-apoptotic. In this study, we overexpressed ?Np73 beta 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 Delta Np73 beta 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 Delta Np73 beta-cells than mock-transfected cells. However, Delta Np73 beta overexpression did not affect the cellular susceptibility to cisplatin. In conclusion, the overexpression of Delta Np73 beta increases viability in p53 wild type and p53 mutant colon cancer cells, and cisplatin induces the degradation of Delta Np73 beta in a dose-dependent manner.

Place, publisher, year, edition, pages
Wiley-Blackwell , 2012. Vol. 51, no 8, 628-635 p.
Keyword [en]
cell death; HCT116 cells; HT29 cells; p73 protein; p53
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Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-79660DOI: 10.1002/mc.20835ISI: 000305962400004OAI: oai:DiVA.org:liu-79660DiVA: diva2:544302
Available from: 2012-08-14 Created: 2012-08-13 Last updated: 2017-12-07

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Pfeifer, DaniellaDing, Zhen-YuSun, Xiao-Feng

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OncologyFaculty of Health SciencesDepartment of Clinical and Experimental MedicineDepartment of Oncology UHL
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Molecular Carcinogenesis
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