Background Acute erythroleukemia (AEL) is an infrequent subtype of acute myeloid leukemia (AML) with worse prognosis. Though the last decade has seen major advances in the novel features and genomic landscape in AEL, there is still a lack of specific therapeutic targets and effective treatment approaches for this disease.MethodsTCGA database was used to screen out the oncogene with specifically aberrant expression in AEL. Protein array was performed to explore the activated signaling pathways

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... d targets that undergo phosphorylation modulation. A series of functional analyses in cell lines and mice models were performed to investigate the biological significance and clinical relevance of KEL regulation in AEL. CHIP, EMSA and dual-luciferase activity assay were performed to explore the upstream regulation mechanism of KEL.ResultsIn this study, the results showed that KEL promoted cell proliferation and its downregulation reversed drug resistance in AEL cells to JQ1. Our findings suggested that KEL contributed to gain of H3K27 acetylation and promoted erythroid differentiation induced by GATA1. Additionally, GATA1 and TAL1 as co-Transcription factors (TFs) modulated the expression of KEL. Maintaining cell viability and differentiation, KEL also played parts in the immune evasion of tumor cells.ConclusionsOur work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, offering promising therapeutic target to broaden the treatment options.