P53 Calls upon CIA (Calcium Induced Apoptosis) to Counter Stress.

Ygal Haupt,Sue Haupt,Dinesh Raghu

doi:10.3389/fonc.2015.00057

Abstract

GENERAL COMMENTARY article Front. Oncol., 10 March 2015Sec. Molecular and Cellular Oncology https://doi.org/10.3389/fonc.2015.00057

Highlights

Intravital imaging reveals p53-dependent cancer cell death induced by phototherapy via calcium signaling by Giorgi C, Bonora M, Missiroli S, Poletti F, Ramirez FG, Morciano G, et al Oncotarget (2015) 6(3)
Over the past two decades, the cytoplasmic tumor suppressive functions of p53 have been studied, revealing a role for cytoplasmic p53 in mitochondrial apoptosis and in the suppression of autophagy, which acts as a survival mechanism under metabolic stress conditions [reviewed in Ref. (4)]
They show that in response to stresses, wild type p53 accumulates at the endoplasmic reticulum–mitochondrial-associated membranes (ER–MAMs), where it interacts with sarco-endoplasmic reticulum Ca2+ ATPase (SERCA) pump to promote calcium overload in the mitochondria

Summary

Introduction

Intravital imaging reveals p53-dependent cancer cell death induced by phototherapy via calcium signaling by Giorgi C, Bonora M, Missiroli S, Poletti F, Ramirez FG, Morciano G, et al Oncotarget (2015) 6(3):1435–45. While the transcriptional activity of p53 is important for its apoptotic function, an early study provided vital direct indication that a transcriptional deficient p53 mutant is able to induce cell death (3). Over the past two decades, the cytoplasmic tumor suppressive functions of p53 have been studied, revealing a role for cytoplasmic p53 in mitochondrial apoptosis and in the suppression of autophagy, which acts as a survival mechanism under metabolic stress conditions [reviewed in Ref.

Results

Conclusion