MicroRNA‑195‑5p inhibits the progression of hemangioma via targeting SKI
- Bin Sun
- Zhi Huang
- Hua Yang
- Xuya Zhao
Affiliations: Department of Neurosurgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550002, P.R. China, School of Basic Medical Science, Guizhou Medical University Guizhou Medical University, Guiyang, Guizhou 550002, P.R. China, Department of Interventional Radiology, The Affiliated Cancer Hospital of Guizhou Medical University, Guiyang, Guizhou 550002, P.R. China
- Published online on: December 22, 2021 https://doi.org/10.3892/etm.2021.11088
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Hemangioma (HA), which is characterized by aberrant endothelial cell proliferation in blood vessels, is a common tumor during infancy. MicroRNAs (miRNAs/miRs) collectively participate in the development of HA; however, the potential roles of miR‑195‑5p in HA are not completely understood. The aim of the present study was to investigate the roles of miR‑195‑5p in HA. In the present study, miR‑195‑5p was found to be downregulated in HA cells, such as the XPTS‑1 human infantile hemangioma‑derived endothelial cell line and the EOMA hemangioendothelioma cell line. Overexpression of miR‑195‑5p was shown to suppress HA cell viability, colony formation and proliferation, and induced HA cell apoptosis. Furthermore, miR‑195‑5p downregulated Bcl‑2 expression and upregulated Bax and Bcl‑2 expression levels. V‑ski sarcoma viral oncogene homolog (SKI) was identified as a target of miR‑195‑5p. Co‑transfection of miR‑195‑5p mimics and SKI 3'‑untranslated region wild‑type decreased HA cell luciferase activity. SKI overexpression alleviated the miR‑195‑5p‑induced decrease in HA cell proliferation and increased HA cell apoptosis. In addition, the regulatory role of miR‑195‑5p on the expression of Bcl‑2, Bax and poly(ADP‑ribose) polymerase was reversed by SKI. Collectively, the results of the present study demonstrated that miR‑195‑5p suppressed HA progression and its effects were mediated via SKI. Therefore, the miR‑195‑5p/SKI axis may represent a novel therapeutic target for HA.