DFFB suppresses interferon to enable cancer persister cell regrowth.

ABSTRACT: Oncogene targeted cancer therapies can provide deep responses but frequently suffer from acquired resistance.¹ Therapeutic approaches to treat tumours which have acquired drug resistance are complicated by continual tumour evolution and multiple co-occurring resistance mechanisms.^2,3 Rather than treating resistance after it emerges, it may possible to prevent it by inhibiting the adaptive processes which initiate resistance but these are poorly understood.⁴ Here we report that residual cancer persister cells that survive oncogene targeted therapy are growth arrested by drug stress-induced intrinsic Type I interferon (IFN) signaling. To escape growth arrest, persister cells leverage apoptotic machinery to transcriptionally suppress interferon-stimulated gene

SUBMITTER: Williams AF 

PROVIDER: S-EPMC12393451 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature