Department of Molecular Biology and Genetics, Erzurum Technical University, Erzurum, Turkey.
Molecular Cancer Biology Laboratory, High Technology Application and Research Center, Erzurum Technical University, Erzurum, Turkey.
Head Neck. 2023 Sep;45(9):2259-2273. doi: 10.1002/hed.27460. Epub 2023 Jul 14.
Oral squamous cell carcinoma (OSCC) is characterized by enhanced angiogenesis resulting in poor prognosis despite improvements in diagnostic/therapeutic techniques. Here, we aimed at investigating potential roles of miR-1825 enclosed in OSCC-derived exosomes on angiogenesis under hypoxic conditions.
Effects of miR-1825 mimic/inhibitor as well as hypoxia-induced tumor derived exosomes on human umbilical vein endothelial cells (HUVECs) were evaluated using cell viability, migration/invasion, tube formation, and spheroid-based 3D angiogenesis assays.
Hypoxic conditions caused significant increase in miR-1825 levels in OSCC cells and hiTDEs. miR-1825 alone and within hiTDEs promoted endothelial cell viability, migration, invasion, and angiogenic potential, which is reversed via inhibition of miR-1825 expression. miR-1825 within hiTDEs altered the angiogenesis potential of HUVEC cells via deregulation of TSC2/mTOR axis.
We showed that hypoxia led to OSCC-derived exosome mediated transfer of miR-1825 to HUVECs and enhanced angiogenesis in OSCC in vitro.
口腔鳞状细胞癌（OSCC）的特点是血管生成增强，尽管诊断/治疗技术有所提高，但预后仍较差。在这里，我们旨在研究缺氧条件下 OSCC 来源的外泌体中包含的 miR-1825 对血管生成的潜在作用。
使用细胞活力、迁移/侵袭、管形成和基于球体的 3D 血管生成测定，评估 miR-1825 模拟物/抑制剂以及缺氧诱导的肿瘤衍生外泌体对人脐静脉内皮细胞（HUVEC）的影响。
缺氧条件导致 OSCC 细胞和 hiTDEs 中 miR-1825 水平显著增加。miR-1825 单独和在 hiTDEs 中促进内皮细胞活力、迁移、侵袭和血管生成潜力，通过抑制 miR-1825 表达可逆转这种作用。hiTDEs 中的 miR-1825 通过调节 TSC2/mTOR 轴改变了 HUVEC 细胞的血管生成潜力。
我们表明，缺氧导致 OSCC 衍生的外泌体介导 miR-1825 转移到 HUVEC，并在体外增强了 OSCC 的血管生成。
