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Published on: October 4, 2019
Identification of novel p53 target genes by cDNA AFLP in glioblastoma cells
Mojtaba Saffari1, Orkideh Saydi Dinehkabodi, Seyed Hamid Ghaffari
1Department of Medical Genetics, Tehran University of Medical Sciences, Pour Sina Avenue, Tehran, Iran.
Abstract:
The p53 plays critical role in cellular functions such as cell cycle arrest and apoptosis. We overexpressed wild-type p53 (wt-p53) in U87 glioblastoma cells via recombinant adenovirus Ad-GFP-P53 which encodes p53 and green fluorescent protein. The transcript profiles were investigated using cDNA amplified fragment length polymorphism approach. Semi-quantitative RT-PCR and DNA sequencing results for the selected genes showed that Cathepsin B and cell cycle associated protein-1 or Caprin-I, genes were suppressed whereas Annexin-II gene overexpressed in response to the overexpression of wt-p53 gene. Our results suggest that these genes could be important mediators of p53-dependent tumor growth suppression in glioblastoma.
Insights
Overexpressing wild-type p53 (wt-p53) in glioblastoma cells suppressed Cathepsin B and Caprin-I genes while overexpressing Annexin-II. These genes may mediate p53-driven tumor growth suppression.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- The p53 tumor suppressor protein is crucial for regulating cell cycle arrest and apoptosis.
- Glioblastoma is an aggressive brain tumor with complex genetic alterations.
- Understanding p53's role in glioblastoma is vital for developing targeted therapies.
Purpose of the Study:
- To investigate the effect of wild-type p53 (wt-p53) overexpression on gene expression in U87 glioblastoma cells.
- To identify potential mediators of p53-dependent tumor growth suppression.
- To explore the molecular mechanisms underlying p53's function in glioblastoma.
Main Methods:
- Overexpression of wt-p53 in U87 glioblastoma cells using a recombinant adenovirus (Ad-GFP-P53).
- Transcript profiling using cDNA amplified fragment length polymorphism (cDNA-AFLP).
- Validation of gene expression changes using semi-quantitative RT-PCR and DNA sequencing.
Main Results:
- Overexpression of wt-p53 led to the suppression of Cathepsin B and cell cycle associated protein-1 (Caprin-I) gene expression.
- Annexin-II gene expression was found to be upregulated in response to wt-p53 overexpression.
- Specific gene expression changes were observed in glioblastoma cells following wt-p53 introduction.
Conclusions:
- Cathepsin B, Caprin-I, and Annexin-II are potential downstream effectors of p53 signaling in glioblastoma.
- These identified genes may play significant roles in mediating the tumor suppressor functions of p53.
- Further research into these genes could reveal novel therapeutic targets for glioblastoma treatment.
