Cross-talk between mutant p53 and p62/SQSTM1 augments cancer cell migration by promoting the degradation of cell adhesion proteins.

doi:10.1073/pnas.2119644119

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Article

Cross-talk between mutant p53 and p62/SQSTM1 augments cancer cell migration by promoting the degradation of cell adhesion proteins.

Proceedings of the National Academy of Sciences of the United States of America - 26 Apr 2022

Mukherjee Saptaparna, Maddalena Martino, Lü YiQing, Martinez Sebastien, Nataraj Nishanth Belugali, Noronha Ashish, Sinha Sansrity, Teng Katie, Cohen-Kaplan Victoria, Ziv Tamar, Arandkar Sharathchandra, Hassin Ori, Chatterjee Rishita, Pirona Anna-Chiara, Shreberk-Shaked Michal, Gershoni Anat, Aylon Yael, Elazar Zvulun, Yarden Yosef, Schramek Daniel, Oren Moshe

Abstract excerpt

Missense mutations in the p53 tumor suppressor abound in human cancer. Common (“hotspot”) mutations endow mutant p53 (mutp53) proteins with oncogenic gain of function (GOF), including enhanced cell migration and invasiveness, favoring cancer progression. GOF is usually attributed to transcriptional effects of mutp53. To elucidate transcription-independent effects of mutp53, we characterized the protein...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 35439056
DOI: 10.1073/pnas.2119644119
PMCID: PMC9173583

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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