Mutant p53 regulates cancer cell invasion in complex three-dimensional environments through mevalonate pathway–dependent Rho/ROCK signaling

A Asja Guzman (Department of Biological Sciences, Columbia University) T Tatsuya Kawase (Astellas Pharma Inc.) A Alexander J. Devanny (Department of Chemistry, Columbia University) G Gizem Efe (Herbert Irving Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center) R Raúl Navaridas (Herbert Irving Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center) K Karen Yu (Department of Physics, Columbia University) K Kausik Regunath (Department of Biological Sciences, Columbia University) I Iris G. Mercer (Department of Chemistry, Columbia University) R Rachel C. Avard (Department of Chemistry, Columbia University) R Rafaela Muniz de Queiroz (Department of Biological Sciences, Columbia University) A Anil K. Rustgi (Herbert Irving Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center) L Laura J. Kaufman (Department of Chemistry) C Carol Prives (Department of Biological Sciences, Columbia University)

Abstract

Certain TP53 mutations can confer neomorphic gain of function (GOF) activities to the p53 protein that affect cancer progression. Yet the concept of mutant p53 GOF has been challenged. Here, using various strategies to alter the status of mutant versions of p53 in different cell lines, we demonstrate that mutant p53 stimulates cancer cell invasion in three-dimensional environments. Mechanistically, mutant p53 enhances RhoA/ROCK-dependent cell contractility and cell-mediated extracellular matrix (ECM) reorganization via increasing mevalonate pathway–dependent RhoA localization to the membrane. In line with this, RhoA-dependent proinvasive activity is also mediated by IDI-1, a mevalonate pathway product. Further, the invasion-enhancing effect of mutant p53 is dictated by the biomechanical properties of the surrounding ECM, thereby adding a cell-independent layer of regulation to mutant p53 GOF activity that is mediated by dynamic reciprocal cell–ECM interactions. Together our findings link mutant p53 metabolic GOF activity with a context-dependent invasive cellular phenotype.

Article Details

Volume / Issue Vol. 122, Issue 43
Published October 28, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (13)

A

Asja Guzman

Department of Biological Sciences, Columbia University

T

Tatsuya Kawase

Astellas Pharma Inc.

A

Alexander J. Devanny

Department of Chemistry, Columbia University

G

Gizem Efe

Herbert Irving Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center

R

Raúl Navaridas

Herbert Irving Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center

K

Karen Yu

Department of Physics, Columbia University

K

Kausik Regunath

Department of Biological Sciences, Columbia University

I

Iris G. Mercer

Department of Chemistry, Columbia University

R

Rachel C. Avard

Department of Chemistry, Columbia University

R

Rafaela Muniz de Queiroz

Department of Biological Sciences, Columbia University

A

Anil K. Rustgi

Herbert Irving Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center

L

Laura J. Kaufman

Department of Chemistry

C

Carol Prives

Department of Biological Sciences, Columbia University