The knockdown of MALAT1 inhibits the proliferation,invasion and migration of hemangioma endothelial cells by regulating MiR-206 / VEGFA axis |
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| Affiliation: | 1. Department of Gynecology and Obstetrics, Affiliated Shenzhen Maternity & Child Healthcare Hospital, Southern Medical University (Shenzhen Maternity & Child Healthcare Hospital), Shenzhen 518028, Guangdong, China;2. Department of Gynecology and Obstetrics, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, Guangdong, China;3. Department of Gynecology and Obstetrics, Shenzhen Hospital, Southern Medical University, Shenzhen 518000, Guangdong, China;1. Department of Clinical Medicine, Women’s Health and Perinatology Research Group, Faculty of Health Sciences, University of Tromsø, Norway;2. Department of Obstetrics and Gynecology, University Hospital of North Norway, Tromsø, Norway;3. Department of Occupational and Environmental Medicine, University Hospital of North Norway, Tromsø, Norway;4. Department of Obstetrics, Oslo University Hospital–Rikshospitalet, Oslo, Norway;5. Department of Clinical Sciences, Intervention, and Technology, Karolinska Institute, Stockholm, Sweden;1. Department of Cell and Tissue Biology, University of California (UCSF), San Francisco, 513 Parnassus Ave, CA 94143, USA;2. University Düsseldorf, Medical Faculty, Department of Obstetrics, Gynecology and REI (UniKiD), Moorenstrasse 5, 40225 Düsseldorf, Germany;3. University Düsseldorf, Medical Faculty, Division of Cardiology, Pulmonology and Vascular Medicine, Moorenstrasse 5, 40225 Düsseldorf, Germany;4. Department of Biology, School of Medicine, Stanford University, Stanford, CA 94305, USA;1. Laboratory Services, Gansu Maternal and Child Health Hospital, Qilihe District, Lanzhou City, Gansu Province 730050, China;2. Obstetrics Department, Baoji Maternal and Child Health Hospital, Baoji City, Shaanxi Province, 721000, China |
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| Abstract: | AimLncRNA MALAT1 is involved in regulation of angiogenesis, however, its expression and mechanism in infantile hemangioma (IH) are less reported. The study aimed to investigate MALAT1 in IH and to reveal the potential mechanism of MALAT1 acting on IH.MethodsIsolated form IH tissue, human CD31+ hemangioma endothelial cells (HemECs) were cultured and sorted by magnetic-activated cell sorting (MACS). Quantitative real-time (qRT)-PCR was performed to detect the expressions of MALAT1, miR-206 and VEGFA. The correlations among MALAT1, miR-206 and VEGFA were confirmed by bioinformatics analysis and dual-luciferase reporter assay. The effects of MALAT1, miR-206 and VEGFA on cell proliferation were detected by cell counting kit-8 (CCK-8) and cell colony formation assay. Flow cytometry, wound scratch, Transwell and Tube formation assay were performed to determine cell apoptosis, migration, invasion and vasoformation, respectively. Apoptosis-related proteins were determined by Western blot.ResultsThe results showed that MALAT1 and VEGFA were high-expressed and miR-206 was low-expressed in IH tissues. SiMALAT1 negatively affected the cell proliferation, migration, invasion and vasoformation of HemECs and promoted apoptosis of HemECs. Moreover, Bcl-2 expression was significantly inhibited and the expressions of Bax and c cleaved-3 were greatly promoted. MALAT1 directly targeted and inhibited the expression of miR-206, and VEGFA was predicted to be the target gene for miR-206. SiMALAT1 suppressed the cell proliferation, migration, invasion and vasoformation of HemECs through modulating miR-206/VEGFA axis.ConclusionKnock-down of MALAT1 inhibits the growth of HemECs through regulating miR-206/VEGFA axis, indicating that MALAT1 is a potential therapeutic mechanism for the treatment of IH. |
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| Keywords: | LncRNA MALAT1 MiR-206 Vascular endothelial growth factor A Infantile hemangioma Human hemangioma endothelial cell |
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