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Published on: May 5, 2023
Epigenetic modification in the expression of p73 p73 - epigenetic target for anticancer therapy
Faiza Naseer1, Mohammad Saleem2
1Shifa College of Pharmaceutical Sciences, Shifa Tameer e Millat University, Islamabad, Pakistan.
Abstract:
A p73 is a new member of p53 family of transcription factor, having two types. First is TAp73, transcriptionally active and expressed via upstream promoter as a tumor suppressor and vital apoptotic inductor, it also has a key role in cell cycle arrest/differentiation and Second is ΔNp73 that is transcriptionally inactive and expressed via downstream regulator as oncogenes. Both types are expressed in various isoforms, which originate from alternative splicing events at the C-terminus. Upon DNA damage, posttranslational modifications cause conformational changes in various amino acid residues via induction or inhibition of various proteins, which are present in the structural domains of p73. These modifications may cause up- or down-regulation of p73 expression levels, as well as alters the transcriptional activity and/or stability of the protein. In this review, we have made an effort to assemble all existing data regarding the role of p73, its modification and after effects in cancer.
Insights
The p73 protein, a p53 family member, has tumor-suppressing (TAp73) and oncogenic (ΔNp73) forms. Posttranslational modifications influence p73
Area of Science:
- Molecular Biology
- Cancer Biology
- Genetics
Background:
- The p53 family includes p73, a transcription factor with tumor suppressor and oncogenic roles.
- p73 exists as TAp73 (active, tumor suppressor) and ΔNp73 (inactive, oncogene).
- Alternative splicing generates various p73 isoforms.
Purpose of the Study:
- To review the role of p73 in cancer.
- To summarize p73 modifications and their effects.
- To consolidate current knowledge on p73's function and regulation.
Main Methods:
- Literature review of existing data on p73.
- Analysis of p73 family members, isoforms, and functions.
- Examination of posttranslational modifications and their impact on p73.
Main Results:
- TAp73 acts as a tumor suppressor, inducing apoptosis and cell cycle arrest.
- ΔNp73 functions as an oncogene.
- Posttranslational modifications alter p73 expression, activity, and stability.
- Isoform diversity arises from alternative splicing.
Conclusions:
- p73 plays a critical role in cancer through its distinct isoforms and regulatory mechanisms.
- Understanding p73 modifications is key to comprehending its function in tumorigenesis.
- This review provides a comprehensive overview of p73's involvement in cancer.
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