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Significance Targeting stem-like cells in cancer is critical to overcoming resistance and relapse post chemotherapy or immunotherapy. We elucidate an alternative-splicing driven mechanism of cancer dedifferentiation and define a molecular context wherein stem-like tumor cells show enhanced susceptibility to JNK inhibition. MBNL1 andMAP2K7 ∆exon2 can prognosticate patients for JNK inhibition that can render stem-like tumor cells susceptible to therapy.

A tumor-associated splice-isoform of MAP2K7 drives dedifferentiation in MBNL1-low cancers via JNK activation