Caspase 2 and p53 Reunited in Tumor Control

Giulia Petroni; Ilio Vitale; Lorenzo Galluzzi

doi:10.1016/j.tcb.2020.09.001

Caspase 2 and p53 Reunited in Tumor Control

Trends Cell Biol. 2020 Dec;30(12):917-918. doi: 10.1016/j.tcb.2020.09.001. Epub 2020 Sep 11.

Authors

Giulia Petroni¹, Ilio Vitale², Lorenzo Galluzzi³

Affiliations

¹ Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
² IIGM - Italian Institute for Genomic Medicine, c/o IRCSS Candiolo, Torino, Italy; Candiolo Cancer Institute, FPO - IRCCS, Candiolo, Italy.
³ Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA; Sandra and Edward Meyer Cancer Center, New York, NY, USA; Caryl and Israel Englander Institute for Precision Medicine, New York, NY, USA; Department of Dermatology, Yale University School of Medicine, New Haven, CT, USA; Université de Paris, Paris, France. Electronic address: deadoc80@gmail.com.

PMID: 32921524
DOI: 10.1016/j.tcb.2020.09.001

Abstract

Recent findings (Tsabar et al.) demonstrate that human cancer cells that evade the cell cycle blockage normally imposed by DNA damage experience sustained p53 signaling upon MDM2 degradation by caspase 2. Such a response may be connected to the delivery of immunostimulatory signals to ensure the elimination of genetically instable cancer cells.

Keywords: CDK4/CDK6 inhibitors; MDM2; PIDD1; double-stand DNA breaks; ionizing radiation; type I interferon.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Apoptosis
Caspase 2 / genetics
Cell Cycle Checkpoints
DNA Breaks, Double-Stranded
DNA Damage
Humans
Neoplasms* / genetics
Proto-Oncogene Proteins c-mdm2 / genetics
Proto-Oncogene Proteins c-mdm2 / metabolism
Radiation, Ionizing
Tumor Suppressor Protein p53* / genetics

Substances

Tumor Suppressor Protein p53
Proto-Oncogene Proteins c-mdm2
Caspase 2