Background: Endometrial carcinoma (EC) development is associated with dysregulated circular RNA profiles. The purpose of the current research is to study the role and mechanism of hsa_circ_0001610 (circ_0001610) in EC progression.
Methods: circ_0001610, microRNA (miR)-646, and signal transducer and activator of transcription 3 (STAT3) expression levels were measured in EC. Functional analyses were performed using Cell Counting Kit-8, colony formation, transwell, wound healing, flow cytometry, glycolysis, and xenograft analyses. Binding association was evaluated with dual-luciferase reporter assay.
Results: circ_0001610 levels were upregulated in EC samples (n = 30) and cells. circ_0001610 interference restrained cell proliferation, migration, and invasion, and promoted apoptosis. circ_0001610 downregulation constrained glycolysis through reducing glucose consumption, lactate production, and levels of adenosine triphosphate, extracellular acidification, hexokinase 2, and lactate dehydrogenase A, and increasing oxygen consumption rate. miR-646 is targeted by circ_0001610, and miR-646 inhibition attenuated interference of circ_0001610-mediated suppression of EC development. STAT3 was modulated by miR-646, and miR-646 upregulation restrained EC progression by decreasing STAT3. circ_0001610 silencing reduced STAT3 levels by sponging miR-646 and reduced the growth of xenograft tumor established by EC cells.
Conclusion: circ_0001610 knockdown represses EC progression through modulating the miR-646-STAT3 axis.
Keywords: STAT3; endometrial carcinoma; glycolysis; hsa_circ_0001610; miR-646.
© 2021 John Wiley & Sons, Ltd.