UHRF1 regulates the transcriptional repressor HBP1 through MIF in T acute lymphoblastic leukemia
نویسندگان
چکیده
Macrophage migration inhibitory factor (MIF) has been confirmed as an oncogene in solid tumor development, and its overexpression causes cell proliferation T acute lymphoblastic leukemia (T?ALL); however, the underlying mechanisms remain unclear. The of MIF promotes cellular transformation proliferation, part, through interaction with UHRF1. Nevertheless, UHRF1 cannot upregulate MIF expression T?ALL. New insights into regulation T?ALL are imperative to offer opportunity for therapeutic intervention. In present study, using RT?qPCR, western blot analysis, confocal microscopy RNA sequence, we report identification validation a negative regulator MIF, which functions downregulate by binding CATT repeat sequence promoter. By contrast, HMG?box protein 1 (HBP1) positive MIF. Moreover, demonstrated that HBP1 suppressive signaling is reduced promotion between HBP1. deficiency caused UHRF1 knockdown resulted enhanced apoptosis compared decreased or increased alone. These results identify key transcription T?ALL, although these factors possess opposite regulatory functions. Thus, this mechanism may provide insight how effectively prevent MIF?dependent oncogenic activity. Finally, mice possessing high low levels associated longer survival control mice, UHRF1?knockdown living longest. Taken together, findings indicate regulators potential treatment targets biomarkers prediction prognosis
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ژورنال
عنوان ژورنال: Oncology Reports
سال: 2021
ISSN: ['1791-2431', '1021-335X']
DOI: https://doi.org/10.3892/or.2021.8082