AIM LncRNA 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. METHODS Isolated 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. RESULTS The 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. CONCLUSION Knock-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.

中文翻译：

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敲低MALAT1可通过调节MiR-206 / VEGFA轴来抑制血管瘤内皮细胞的增殖，侵袭和迁移。

AIM LncRNA MALAT1参与血管生成的调控，但是，其在婴儿血管瘤（IH）中的表达和机制尚鲜见报道。该研究旨在调查IH中的MALAT1，并揭示MALAT1作用于IH的潜在机制。方法从IH组织中分离培养人CD31 +血管瘤内皮细胞（HemEC），并通过磁激活细胞分选术（MACS）进行分选。进行定量实时（qRT）-PCR以检测MALAT1，miR-206和VEGFA的表达。通过生物信息学分析和双荧光素酶报告基因分析证实了MALAT1，miR-206和VEGFA之间的相关性。通过细胞计数试剂盒8（CCK-8）和细胞集落形成试验检测MALAT1，miR-206和VEGFA对细胞增殖的影响。流式细胞仪，伤口刮伤，进行Transwell和试管形成测定，分别测定细胞凋亡，迁移，侵袭和血管形成。通过Western印迹测定凋亡相关蛋白。结果结果显示，在IH组织中MALAT1和VEGFA高表达，而miR-206低表达。SiMALAT1对HemECs的细胞增殖，迁移，侵袭和血管形成有负面影响，并促进HemECs的凋亡。而且，Bcl-2表达被显着抑制，Bax和c cleaved-3的表达被大大促进。MALAT1直接靶向并抑制miR-206的表达，而VEGFA被预测为miR-206的靶基因。SiMALAT1通过调节miR-206 / VEGFA轴抑制了HemEC的细胞增殖，迁移，侵袭和血管形成。