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Related Experiment Video

Updated: May 24, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

p53/HMGB1 complexes regulate autophagy and apoptosis.

Kristen M Livesey¹, Rui Kang, Philip Vernon

¹Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania 15213, USA.

Cancer Research

|February 21, 2012

Summary

This summary is machine-generated.

High mobility group box 1 (HMGB1) and p53 form a complex regulating cell death and survival. HMGB1 promotes autophagy when p53 is diminished, impacting tumor cell survival and carcinogenesis.

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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Area of Science:

Molecular Biology
Cell Biology
Cancer Research

Background:

Apoptosis (programmed cell death) and autophagy (programmed cell survival) are critical in tumor development and therapy.
The interplay between these processes influences cancer progression and treatment outcomes.

Purpose of the Study:

To investigate the role of high mobility group box 1 (HMGB1) and p53 in regulating the balance between apoptosis and autophagy.
To elucidate the molecular mechanisms by which HMGB1 and p53 interact to control cell fate.

Main Methods:

Utilized gene knockout techniques (p53 and HMGB1) in cell lines (HCT116) and primary cells (mouse embryonic fibroblasts).
Assessed the expression and localization of HMGB1 and p53.
Quantified levels of autophagy and apoptosis.

Main Results:

p53 knockout increased cytosolic HMGB1 expression and induced autophagy.
HMGB1 knockout increased p53 cytosolic localization and decreased autophagy.
p53 acts as a negative regulator of the HMGB1/Beclin 1 complex.
HMGB1 promotes autophagy in conditions of reduced p53 function, supporting tumor cell survival.

Conclusions:

A novel link between HMGB1 and p53 in the cross-regulation of apoptosis and autophagy under cell stress was identified.
The HMGB1/p53 complex modulates the cytoplasmic localization of binding partners, thereby controlling autophagy and apoptosis.
These findings offer insights into the reciprocal roles of HMGB1 and p53 in carcinogenesis.