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Data from: Inhibition of p38-MK2 pathway enhances the efficacy of microtubule inhibitors in breast cancer cells

Data files

Apr 06, 2026 version files 114.11 KB

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Abstract

These datasets support the following findings: Microtubule-targeting agents (MTAs) are widely used in cancer therapy, but their benefits are limited to subsets of patients and are often associated with toxicity in normal cells. This highlights the need for strategies that improve MTA efficacy while reducing side effects. Here, we show that inhibition of the p38 MAPK-MK2 pathway sensitizes cancer cells to MTAs. We identify CMPD1 as a dual-target inhibitor that suppresses p38-MK2 signaling and disrupts microtubule dynamics by rapidly inducing plus-end microtubule depolymerization. CMPD1 inhibits tumor growth and invasion in vitro and in vivo, and at 10 nM induces irreversible mitotic defects selectively in cancer cells, sparing non-transformed cells. We further show that a specific p38-MK2 inhibitor enhances the efficacy of subclinical MTA doses. These findings support p38-MK2 inhibition as a promising strategy to improve MTA-based cancer treatment.