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

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.