Abstract
The p53 family consists of three members: p53, p63 and p73. All three of them have a role in cell cycle arrest and induction of apoptosis. However, despite structural and partly functional similarity, there are striking differences in their functions and each of them has its own and unique identity. All three genes encode multiple variants with opposing functions in cancer development – full length transactivation forms with proapoptotic and antiproliferative functions, and dominant-negative transactivation-deficient forms with antiapoptotic (oncogenic) functions. The functional interactions between family members are crucial to gain insight and understand their role in cancer biology. The discovery of p53/p73 network could have a major clinical impact in prognostic use and targeted drug design. In the current review we present the recent achievements in p73 research including very complex and sophisticated p73 regulation and response to DNA damage, and functional interactions among family members. We discuss how p73 has affected drug discovery. According to the p73 tumor suppressor function, we outline current aspects of anticancer therapy.
Keywords: p73, apoptosis, cancer, chemosensitivity, cancer therapy, breast cancer, TAp73, carboxy-terminal, Proteins, DNA-damaging, hetero-oligomers, dominant-negative, inhibitor, coexpression, Coimmunoprecipitation, fetoprotein, posttranslational, E2F1
Current Pharmaceutical Design
Title: Targeting p73 - a Potential Approach in Cancer Treatment
Volume: 17 Issue: 6
Author(s): Neda Slade and Andela Horvat
Affiliation:
Keywords: p73, apoptosis, cancer, chemosensitivity, cancer therapy, breast cancer, TAp73, carboxy-terminal, Proteins, DNA-damaging, hetero-oligomers, dominant-negative, inhibitor, coexpression, Coimmunoprecipitation, fetoprotein, posttranslational, E2F1
Abstract: The p53 family consists of three members: p53, p63 and p73. All three of them have a role in cell cycle arrest and induction of apoptosis. However, despite structural and partly functional similarity, there are striking differences in their functions and each of them has its own and unique identity. All three genes encode multiple variants with opposing functions in cancer development – full length transactivation forms with proapoptotic and antiproliferative functions, and dominant-negative transactivation-deficient forms with antiapoptotic (oncogenic) functions. The functional interactions between family members are crucial to gain insight and understand their role in cancer biology. The discovery of p53/p73 network could have a major clinical impact in prognostic use and targeted drug design. In the current review we present the recent achievements in p73 research including very complex and sophisticated p73 regulation and response to DNA damage, and functional interactions among family members. We discuss how p73 has affected drug discovery. According to the p73 tumor suppressor function, we outline current aspects of anticancer therapy.
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Cite this article as:
Slade Neda and Horvat Andela, Targeting p73 - a Potential Approach in Cancer Treatment, Current Pharmaceutical Design 2011; 17 (6) . https://dx.doi.org/10.2174/138161211795222621
DOI https://dx.doi.org/10.2174/138161211795222621 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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