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- W3146291954 abstract "Abstract 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. Methods TCGA database was used to screen out the oncogene with specifically aberrant expression in AEL. Protein array was performed to explore the activated signaling pathways and 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. Results In 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. Conclusions Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, offering promising therapeutic target to broaden the treatment options." @default.
- W3146291954 created "2021-04-13" @default.
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- W3146291954 date "2021-04-06" @default.
- W3146291954 modified "2023-10-16" @default.
- W3146291954 title "Functional Evaluation of KEL As An Oncogenic Gene in The Progression of Acute Erythroleukemia" @default.
- W3146291954 doi "https://doi.org/10.21203/rs.3.rs-381817/v1" @default.
- W3146291954 hasPublicationYear "2021" @default.
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