MicroRNA‑203a‑3p suppresses endothelial cell proliferation and invasion, and promotes apoptosis in hemangioma by inactivating the VEGF‑mediated PI3K/AKT pathway
- Zhenfeng Hu
- Lei Zhuo
- Yanling Li
- Dongpeng Duan
- Jing Guo
Affiliations: Department of General Surgery II (Department of Plastic Surgery), Affiliated Hospital of Hebei University of Engineering, Handan, Hebei 056002, P.R. China, Department of General Surgery Ⅳ (Department of Plastic Surgery), Affiliated Hospital of Hebei University of Engineering, Handan, Hebei 056002, P.R. China, Functional Inspection Department, Handan Ming Ren Hospital, Handan, Hebei 056006, P.R. China, Department of Emergency, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei 056002, P.R. China, The Fourth Ward of Cardiovascular Medicine Department, Handan Central Hospital, Handan, Hebei 056002, P.R. China
- Published online on: September 1, 2022 https://doi.org/10.3892/etm.2022.11581
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Our previous study demonstrated that microRNA-203a‑3p (miR‑203a‑3p) was involved in the regulation of long non‑coding RNA MEG8‑mediated the progression of hemangioma, which is a benign tumor characterized by endothelial hyperplasia in the blood vessels and primarily occurring in infants and females. Therefore, the present study aimed to further investigate the effects of miR‑203a‑3p on endothelial cell proliferation, invasion and apoptosis, as well as its underlying mechanism in hemangioma. Human hemangioma endothelial cells (HemECs) were first transfected with either miR‑203a‑3p mimics or a miR‑203a‑3p inhibitor. Subsequently, vascular endothelial growth factor A (VEGFA) was overexpressed in these cells. Cell proliferation (by Cell Counting Kit‑8 assay), apoptosis (by TUNEL assay), invasion (by Transwell assay) and PI3K/AKT signaling (by western blot) were assessed following transfection of these cells. Notably, transfection with miR‑203a‑3p mimics caused a reduction in cell proliferation, invasion and in the phosphorylation levels of PI3K and AKT, and promoted cell apoptosis in HemECs. By contrast, transfection with the miR‑203a‑3p inhibitor exerted the opposite effects compared with those of the miR‑203a‑3p mimics. miR‑203a‑3p was revealed to directly suppress VEGFA expression in HemECs. VEGFA overexpression alone increased cell proliferation and invasion, but decreased apoptosis. Furthermore, VEGFA co‑transfection reversed the effects mediated by miR‑203a‑3p mimics transfection in HemECs. Mechanistically, miR‑203a‑3p was demonstrated to inactivate the PI3K/AKT pathway, whereas VEGFA overexpression produced the opposite effect. VEGFA co‑transfection also attenuated the miR‑203a‑3p mimics‑induced inactivation of PI3K/AKT signaling in HemECs. In conclusion, these data suggested that miR‑203a‑3p may inhibit endothelial cell proliferation and invasion, and promote apoptosis by inactivating VEGFA and PI3K/AKT signaling in hemangioma. These findings also implicated miR‑203 as a possible treatment option for this disease.