In preparation for lactation the ETS transcription factor ELF5 drives cell-fate decisions within the mammary luminal progenitor cell population that force differentiation toward the estrogen receptor negative alveolar cell lineage. In estrogen receptor positive luminal A breast cancer, early disease progression is predicted by high levels of ELF5, and in preclinical models elevated ELF5 is associated with its two key features, the acquisition of resistance to endocrine therapy and increased metastasis. We hypothesized that persistence in luminal A breast cancer of the normal developmental role of ELF5 provides a mechanism by which ELF5 can drive progression to endocrine insensitivity, and here we detail molecular mechanisms by which this may occur. Using chromatin immunoprecipitation sequencing we found that ELF5 binding overlapped with FOXA1 and ER at enhancers and promoters, and when elevated, caused FOXA1 and ER to bind to new regions of the genome involved in resistance to endocrine therapy. RNA sequencing demonstrated that these changes altered estrogen-driven gene expression and the expression of ER transcription-complex members. Using rapid immunoprecipitation mass spectrometry of endogenous proteins and proximity ligation assays we found that ELF5 interacted physically with members of the ER transcription complex, such as DNA-PKcs. These data provide a mechanistic basis by which ELF5 may influence the progression of luminal breast A cancer to endocrine insensitivity.