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Article

Class IIa HDACs forced degradation allows resensitization of oxaliplatin-resistant FBXW7-mutated colorectal cancer.

Molecular oncology - 1 Mar 2026

Tolotto Vanessa, Gualandi Nicolò, Cortolezzis Ylenia, Picco Raffaella, Colitti Monica, D'Este Francesca, Gani Mariachiara, Hancock Wayne W, Terrosu Giovanni, Degrassi Cristina, Agostini Francesca, Brancolini Claudio, Xodo Luigi E, Di Giorgio Eros

Abstract excerpt

Epigenetic plasticity and large-scale chromatin remodeling characterize tumor evolution and the emergence of subclones resistant to conventional therapies. Catalytically inactive class IIa HDACs (HDAC4, HDAC5, HDAC7, HDAC9) control the targeted recruitment of chromatin remodeling complexes, making them attractive therapeutic targets in oncology. In this study, we found that HDAC4 is degraded by the proteasome in...

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Share to Colorectal Neoplasms
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Epigenesis, Genetic

Share to F-Box-WD Repeat-Containing Protein 7

Share to Histone Deacetylases

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Source

Open in PubMed Open full text

Identifiers

PMID: 41174352
DOI: 10.1002/1878-0261.70152
PMCID: PMC13042376

Genes

HDAC4
HDAC5
HDAC7
HDAC9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

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Class IIa HDACs forced degradation allows resensitization of oxaliplatin-resistant FBXW7-mutated colorectal cancer.PMID 41174352Read ↗

Super-enhancers reorganization controls re-sensitization of oxaliplatin-resistant FBXW7-mutated colorectal cancerSemantic proximity Read ↗

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