Targeting mutant p53 stabilization for cancer therapy

نویسندگان

چکیده

Over 50% cancer bears TP53 mutation, the highly stabilized mutant p53 protein drives tumorigenesis and progression. Mutation of not only cause loss-of-function dominant-negative effects (DNE), but also results in abnormal stability by regulation ubiquitin-proteasome system molecular chaperones that promote through gain-of-function effects. The accumulation is mainly regulated chaperones, including Hsp40, Hsp70, Hsp90 other biomolecules such as TRIM21, BAG2 Stat3. In addition, forms prion-like aggregates or complexes with molecules result tumor cells. Depleting has become one strategies to target p53. This review will focus on mechanism stabilization discuss how manipulate these interconnected processes for therapy.

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ژورنال

عنوان ژورنال: Frontiers in Pharmacology

سال: 2023

ISSN: ['1663-9812']

DOI: https://doi.org/10.3389/fphar.2023.1215995