Background
Circular RNAs (circRNAs) play a crucial role in tumorigenesis. However, the effects of circRNAs on acute myeloid leukemia (AML) remain largely unexplored. We explored the function of circRAD18 in AML development.
Methods
QRT-PCR was performed for the levels of circRAD18, RAD18, microRNA-206 (miR-206) and
protein kinase CAMP-activated catalytic subunit beta
(
PRKACB
). Cell Counting Kit-8 (CCK-8) assay and colony formation assay were utilized for cell proliferation. Flow cytometry analysis was carried out to analyze cell apoptosis and cell cycle process. Transwell assay was manipulated for cell migration and invasion. Western blot assay was conducted for protein levels. Dual-luciferase reporter assay was adopted to verify the interaction between miR-206 and circRAD18 or
PRKACB
.
Results
CircRAD18 level was increased in AML patients’ blood specimens and AML cell lines compared to normal controls. CircRAD18 knockdown impeded the proliferation, migration and invasion and facilitated the apoptosis and cell cycle arrest in AML cells. Moreover, circRAD18 was identified as a sponge for miR-206, and circRAD18 knockdown-mediated effect on AML cell progression was reversed by miR-206 suppression. Additionally,
PRKACB
was the target gene of miR-206. MiR-206 overexpression suppressed the malignant behaviors of AML cells, while
PRKACB
elevation restored the effects.
Conclusion
CircRAD18 aggravated the malignancy of AML cells through reducing miR-206 expression and elevating
PRKACB
expression, indicating circRAD18 might be a therapeutic target for AML.
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