Targeting Cell division cycle 37: A Promising Novel Therapeutic Strategy

Cell division cycle 37 (CDC37) is a kinase-specific HSP90 cochaperone that stabilizes oncogenic kinases and is frequently overexpressed in malignancies, making it a compelling therapeutic target. Herein, we systematically delineate therapeutic strategies aimed at inhibiting CDC37, including modulating its Ser13 phosphorylation switch through CK2 inhibition or PP5 activation, disrupting the CDC37-HSP90 complex, and blocking its interaction with kinase clients. These approaches culminate in the concerted degradation of multiple kinase client proteins. CDC37 inhibitors induce cell cycle arrest and apoptosis in models of colon cancer, prostate cancer, and others. Critically, by disrupting the thermal stability of kinases, CDC37-targeting agents can resensitize resistant tumors to kinase inhibitors. In summary, targeting CDC37 is not only a novel anticancer strategy but also a paradigm-shifting approach to address the persistent challenge of kinase inhibitor resistance.

Authors

Institutions

Publication Details

Journal
ChemMedChem
Published
2025-11-30
DOI
https://doi.org/10.1002/cmdc.202500794
Primary Topic
Heat shock proteins research
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Targeting Cell division cycle 37: A Promising Novel Therapeutic Strategy

Qidong You, Lixiao Zhang, Lei Wang, Yi-Xuan Xin
ChemMedChem
Heat shock proteins research
article

Targeting Cell division cycle 37: A Promising Novel Therapeutic Strategy

Qidong You, Lixiao Zhang, Lei Wang, Yi-Xuan Xin
article en

Abstract

Cell division cycle 37 (CDC37) is a kinase-specific HSP90 cochaperone that stabilizes oncogenic kinases and is frequently overexpressed in malignancies, making it a compelling therapeutic target. Herein, we systematically delineate therapeutic strategies aimed at inhibiting CDC37, including modulating its Ser13 phosphorylation switch through CK2 inhibition or PP5 activation, disrupting the CDC37-HSP90 complex, and blocking its interaction with kinase clients. These approaches culminate in the concerted degradation of multiple kinase client proteins. CDC37 inhibitors induce cell cycle arrest and apoptosis in models of colon cancer, prostate cancer, and others. Critically, by disrupting the thermal stability of kinases, CDC37-targeting agents can resensitize resistant tumors to kinase inhibitors. In summary, targeting CDC37 is not only a novel anticancer strategy but also a paradigm-shifting approach to address the persistent challenge of kinase inhibitor resistance.

ChemMedChemVol. 21(1)
China Pharmaceutical University (CN)
Openalex Percentile: Top 66%
Heat shock proteins research
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.