This study is aimed at determining how oral squamous cell carcinoma (OSCC) regulates the angiogenesis of HUVECs through miR-210-3p expression and exploring the relationship among miR-210-3p, its target protein, and the possible mechanism of angiogenesis regulation. miR-210-3p expression was detected in OSCC tissues and juxta cancerous tissues (JCT), and the relationship among miR-210-3p, microvessel density (MVD), and histopathologic features was analyzed. A conditioned medium (CM) of the OSCC cell line CAL27 was collected to stimulate human umbilical vein endothelial cells (HUVECs), and the miR-210-3p levels and tube formation capability of HUVECs were measured. The target protein level of miR-210-3p was altered; then, PI3K/AKT pathway activation in HUVECs was detected. miR-210-3p was tested in exosomes separated from CAL27 CM, and the transfer of miR-210-3p from OSCC exosomes to HUVECs was verified. Then, we found that the OSCC tissues had higher miR-210-3p levels than the JCT, and miR-210-3p level was positively correlated with MVD and tumor grade. CAL27 CM was able to elevate miR-210-3p levels in HUVECs and promoted tube formation. EFNA3 was the target gene of miR-210-3p, and ephrinA3 protein level was able to influence the migration and proliferation of HUVECs. The levels of phosphorylated AKT in the HUVECs increased when ephrinA3 was downregulated, and the upregulation of ephrinA3 resulted in the suppression of the PI3K/AKT pathway. miR-210-3p was detected in exosomes isolated from the CM of CAL27 cells, and miR-210-3p level in the HUVECs was elevated after absorbing the OSCC exosomes. In conclusion, miR-210-3p was more overexpressed in OSCC tissues than in the JCT. The exosomes secreted by OSCC cells were able to upregulate miR-210-3p expression and reduce ephrinA3 expression in HUVECs and promoted tube formation through the PI3K/AKT signaling pathway.

中文翻译：

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OSCC外来体通过PI3K / AKT途径调控靶向EFNA3的miR-210-3p，以促进口腔癌血管生成。

这项研究旨在确定口腔鳞状细胞癌（OSCC）如何通过miR-210-3p表达来调节HUVEC的血管生成，并探讨miR-210-3p，其靶蛋白与血管生成调节的可能机制之间的关系。在OSCC组织和癌旁组织（JCT）中检测到miR-210-3p表达，并分析了miR-210-3p，微血管密度（MVD）和组织病理学特征之间的关系。收集OSCC细胞系CAL27的条件培养基（CM）以刺激人脐静脉内皮细胞（HUVEC），并测量HUVEC的miR-210-3p水平和管形成能力。miR-210-3p的目标蛋白质水平已改变；然后，检测HUVEC中的PI3K / AKT途径活化。在从CAL27 CM分离的外泌体中测试了miR-210-3p，验证了miR-210-3p从OSCC外泌体到HUVEC的转移。然后，我们发现OSCC组织的miR-210-3p水平高于JCT，并且miR-210-3p水平与MVD和肿瘤等级呈正相关。CAL27 CM能够升高HUVEC中的miR-210-3p水平并促进管形成。EFNA3是miR-210-3p的靶基因，ephrinA3蛋白水平能够影响HUVEC的迁移和增殖。当ephrinA3下调时，HUVECs中磷酸化AKT的水平增加，而ephrinA3的上调导致PI3K / AKT途径的抑制。在从CAL27细胞的CM分离的外泌体中检测到miR-210-3p，并且在吸收OSCC外泌体后，HUVEC中的miR-210-3p水平升高。总之，与JCT相比，miR-210-3p在OSCC组织中的过度表达。