| Literature DB >> 30037980 |
Dong-Mei Wu1,2, Xin Wen1,2, Xin-Rui Han1,2, Shan Wang1,2, Yong-Jian Wang1,2, Min Shen1,2, Shao-Hua Fan1,2, Zi-Feng Zhang1,2, Qun Shan1,2, Meng-Qiu Li1,2, Bin Hu1,2, Gui-Quan Chen3, Jun Lu4,2, Yuan-Lin Zheng4,2.
Abstract
In the current study, we were interested in exploring the molecular mechanism of circular RNA DLEU2 (circRNA-DLEU2) (hsa_circ_0000488) and microRNA 496 (miR-496), as well as PRKACB, in human acute myeloid leukemia (AML) cell activities. The RNA expression levels of circRNA-DLEU2, hsa-miR-496, and PRKACB were assessed by quantitative real-time PCR (qRT-PCR). The proliferation and apoptosis abilities of the cells were determined by CCK8 assay and flow cytometry analysis. Target relationships between circRNA-DLEU2 and miR-496, as well as PRKACB, were analyzed by luciferase reporter assay and probe assay. Immunoblotting assays were used to detect the protein expression level of PRKACB. We also did in vivo experiments to observe tumor formation after overexpression of circRNA-DLEU2. Our data showed that circRNA-DLEU2 was upregulated in AML tissues and cells, which promoted AML cell proliferation and inhibited cell apoptosis. circRNA-DLEU2 promoted AML tumor formation in vivo miR-496 was inhibited by circRNA-DLEU2 and was downregulated in AML tissues. circRNA-DLEU2 inhibited miR-496 expression and promoted PRKACB expression. miR-496 antagonized the effects of PRKACB on MOLM-13 cell proliferation and apoptosis. Collectively, circRNA-DLEU2 accelerated human AML by suppressing miR-496 and promoting PRKACB expression.Entities:
Keywords: AML; PRKACB; circRNA-DLEU2; hsa-miR-496
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Year: 2018 PMID: 30037980 PMCID: PMC6168983 DOI: 10.1128/MCB.00259-18
Source DB: PubMed Journal: Mol Cell Biol ISSN: 0270-7306 Impact factor: 4.272