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The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53
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p53 Isoforms and Their Implications in Cancer

Department of Cell and Molecular Biology, Uppsala University, Box-596, BMC, Uppsala SE-75124, Sweden
Author to whom correspondence should be addressed.
Cancers 2018, 10(9), 288;
Received: 22 July 2018 / Revised: 18 August 2018 / Accepted: 18 August 2018 / Published: 25 August 2018
(This article belongs to the Special Issue p53 Signaling in Cancers)
In this review we focus on the major isoforms of the tumor-suppressor protein p53, dysfunction of which often leads to cancer. Mutations of the TP53 gene, particularly in the DNA binding domain, have been regarded as the main cause for p53 inactivation. However, recent reports demonstrating abundance of p53 isoforms, especially the N-terminally truncated ones, in the cancerous tissues suggest their involvement in carcinogenesis. These isoforms are ∆40p53, ∆133p53, and ∆160p53 (the names indicate their respective N-terminal truncation). Due to the lack of structural and functional characterizations the modes of action of the p53 isoforms are still unclear. Owing to the deletions in the functional domains, these isoforms can either be defective in DNA binding or more susceptive to altered ‘responsive elements’ than p53. Furthermore, they may exert a ‘dominant negative effect’ or induce more aggressive cancer by the ‘gain of function’. One possible mechanism of p53 inactivation can be through tetramerization with the ∆133p53 and ∆160p53 isoforms—both lacking part of the DNA binding domain. A recent report and unpublished data from our laboratory also suggest that these isoforms may inactivate p53 by fast aggregation—possibly due to ectopic overexpression. We further discuss the evolutionary significance of the p53 isoforms. View Full-Text
Keywords: p53; cancer; p53 isoform; ∆133p53; ∆160p53; ∆40p53; aggregation; prion p53; cancer; p53 isoform; ∆133p53; ∆160p53; ∆40p53; aggregation; prion
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MDPI and ACS Style

Vieler, M.; Sanyal, S. p53 Isoforms and Their Implications in Cancer. Cancers 2018, 10, 288.

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