作者: Xiaolu Zhang , Jiping Zeng , Minran Zhou , Bingnan Li , Yuanyuan Zhang
关键词: K562 cells 、 RNA interference 、 Cell aging 、 Ectopic expression 、 Cancer research 、 Biology 、 Bone marrow 、 microRNA 、 Azacitidine 、 Immunology 、 Myeloid leukemia
摘要: Background: Recent evidence has accumulated that MicroRNA (miRNA) dysregulation occurs in the majority of human malignancies including acute myeloid leukemia (AML) and may contribute to onco-/leukemo-genesis. Methods: The expression levels miR-370 FoxM1 were assessed 48 newly diagnosed AML patients, 40 patients 1 st complete remission (CR) 21 healthy controls. Quantitative real-time PCR, western blots, colony formation assay, β-Galactosidase ( SA-β-Gal) staining used characterize changes induced by overexpression or inhibition FoxM1. Results: We found down-regulation was a frequent event both cell lines primary leukemic cells from with de novo AML. Lower 37 samples compared those bone marrow derived adult individuals. Ectopic HL60 K562 led growth arrest senescence. In contrast, depletion using RNA interference enhanced proliferation cells. Mechanistically, targets transcription factor FoxM1, well established oncogenic promoting cycle progression. Moreover, when treated 5-aza-2 0 -deoxycytidine, DNA methylation inhibitor, up-regulated, which indicates epigenetic silencing Conclusions: Taken together, function as tumor suppressor targeting silence thus leads derepression consequently contributes development