p53-Mediated Tumor Suppression: DNA-Damage Response and Alternative Mechanisms

Consuelo Pitolli; Ying Wang; Eleonora Candi; Yufang Shi; Gerry Melino; Ivano Amelio

doi:10.3390/cancers11121983

p53-Mediated Tumor Suppression: DNA-Damage Response and Alternative Mechanisms

Cancers (Basel). 2019 Dec 9;11(12):1983. doi: 10.3390/cancers11121983.

Authors

Consuelo Pitolli^{1

2}, Ying Wang³, Eleonora Candi^{1

4}, Yufang Shi^{3

5}, Gerry Melino^{1

2}, Ivano Amelio^{1

2}

Affiliations

¹ Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133 Roma, Italy.
² MRC Toxicology Unit, University of Cambridge, Cambridge CB2 1QP, UK.
³ CAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100012, China.
⁴ IDI-IRCCS, Biochemistry Laboratory, 00133 Rome, Italy.
⁵ Institutes for Translational Medicine, Soochow University, Suzhou 215006, China.

Abstract

The tumor suppressor p53 regulates different cellular pathways involved in cell survival, DNA repair, apoptosis, and senescence. However, according to an increasing number of studies, the p53-mediated canonical DNA damage response is dispensable for tumor suppression. p53 is involved in mechanisms regulating many other cellular processes, including metabolism, autophagy, and cell migration and invasion, and these pathways might crucially contribute to its tumor suppressor function. In this review we summarize the canonical and non-canonical functions of p53 in an attempt to provide an overview of the potentially crucial aspects related to its tumor suppressor activity.

Keywords: cancer; cell death; epigenetics; metabolism.

Publication types

Review

Abstract

Publication types

Grants and funding