Δ133p53β isoform pro-invasive activity is regulated through an aggregation-dependent mechanism in cancer cells

Abstract

p53 isoform Δ133p53β is reported to promote intrinsic oncogenic functions. Here the authors show Δ133p53β is sequestered as aggregates in an inactive form, while association with interacting partners including p63 isoforms and the CCT chaperone complex promotes Δ133p53β activity, resulting in enhanced cancer cell migration and invasion.