Format:
Online-Ressource
ISSN:
2391-5412
Content:
Abstract: Previous research has revealed the involvement of microRNA-212-5p (miR-212-5p) and cyclin T2 (CCNT2) in acute myeloid leukemia (AML). However, whether the miR-212-5p/CCNT2 axis is required for the function of decitabine in AML has not been well elucidated. Quantitative reverse transcription-polymerase chain reaction was used to examine enrichment of miR-212-5p. The relationship between CCNT2 and miR-212-5p was verified by the luciferase reporter assay. Cell apoptosis was evaluated by flow cytometry and western blot. CCK-8 assay was performed to determine cell viability. Decitabine significantly repressed cell viability, while promoted cell apoptosis. Meanwhile, the expression levels of cyclinD1, CDK4, and Bcl-2 were suppressed in cells with decitabine exposure, but Bax and caspase-3 expression levels were upregulated. Besides, miR-212-5p upregulation had the similar function with decitabine in AML cell proliferation and apoptosis. Subsequently, restoration of CCNT2 attenuated miR-212-5p overexpression-induced effects in Kasumi-1 and SKNO-1 cells. In addition, miR-212-5p depletion reversed decitabine-induced CCNT2 downregulation. The miR-212-5p/CCNT2 axis had an implication in the anti-leukemic effect of decitabine in AML.
In:
volume:15
In:
number:1
In:
year:2020
In:
pages:1013-1023
In:
extent:11
In:
Open life sciences, Berlin : De Gruyter, 2015-, 15, Heft 1 (2020), 1013-1023 (gesamt 11), 2391-5412
Language:
English
DOI:
10.1515/biol-2020-0097
URN:
urn:nbn:de:101:1-2409201715548.445234169151
URL:
https://doi.org/10.1515/biol-2020-0097
URL:
https://nbn-resolving.org/urn:nbn:de:101:1-2409201715548.445234169151
URL:
https://d-nb.info/1342576233/34
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