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Effects of ΔNp73β on cisplatin treatment in colon cancer cells
Jasmine Lööf1, Daniella Pfeifer, Zhenyu Ding
1Division of Tumor Biology, Systems Biology Research Centre, University of Skövde, Skövde, Sweden.
Abstract:
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, ΔNp73, which lacks the transactivation domain of the full length TAp73 protein. TAp73 is considered pro-apoptotic, and ΔNp73 anti-apoptotic. In this study, we overexpressed ΔNp73β 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 ΔNp73β 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 ΔNp73β-cells than mock-transfected cells. However, ΔNp73β overexpression did not affect the cellular susceptibility to cisplatin. In conclusion, the overexpression of ΔNp73β increases viability in p53 wild type and p53 mutant colon cancer cells, and cisplatin induces the degradation of ΔNp73β in a dose-dependent manner.
Insights
Overexpression of delta Np73 beta (ΔNp73β) increases colon cancer cell viability. Cisplatin treatment degrades ΔNp73β, but does not alter cellular susceptibility to the drug.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- The p73 gene encodes TAp73 (pro-apoptotic) and ΔNp73 (anti-apoptotic) isoforms.
- ΔNp73 lacks the transactivation domain of TAp73.
- The role of ΔNp73 in colon cancer response to chemotherapy is not fully understood.
Purpose of the Study:
- To investigate the effect of ΔNp73β overexpression on colon cancer cell viability.
- To examine the impact of cisplatin on ΔNp73β expression and colon cancer cell response.
- To determine if ΔNp73β influences cellular susceptibility to cisplatin.
Main Methods:
- Overexpression of ΔNp73β in p53 wild-type and mutant colon cancer cell lines.
- Treatment with cisplatin, a common cancer therapeutic drug.
- Assessment of cell viability, apoptosis, clonogenic potential, and protein expression levels.
Main Results:
- Cisplatin decreased ΔNp73β protein levels in a dose-dependent manner.
- Both TAp73 and p53 protein levels increased following cisplatin treatment.
- ΔNp73β overexpression significantly increased cellular viability but did not affect cisplatin susceptibility.
Conclusions:
- ΔNp73β overexpression enhances viability in both p53 wild-type and mutant colon cancer cells.
- Cisplatin induces dose-dependent degradation of ΔNp73β.
- ΔNp73β does not modulate the sensitivity of colon cancer cells to cisplatin.
