Emerging evidence had highlighted that exosomes could mediate cell-cell communication in human cancerous development via transferring the various molecular cargos, including long non-coding RNA (lncRNA). Taurine up-regulated 1 (TUG1) was previously reported as an oncogenic lncRNA in cervical cancer (CC) via facilitating cell proliferation and other vital biological behaviors. Nevertheless, the presence of TUG1 in exosomes and the functional regulation of exosomal TUG1 in CC are still elusive. The current study aimed at the communication between CC cell lines and endothelial cell-mediated by exosomes, as well as the roles of exosomes derived from CC cells and exosomal TUG1 in affecting angiogenesis. Initially, it was found that TUG1 expression was upregulated in both CC cells and their secreted exosomes. TUG1 was transferred from CC cells to recipient human umbilical vein endothelial cells (HUVECs) in the exosomes way. Interestingly, TUG1 depletion impaired the exosomes-mediated proangiogenic potential of HUVECs by modulating certain key angiogenesis-related genes. In addition, exosomal TUG1 contributed to HUVECs proliferation through suppressing caspase-3 activity and impacting apoptosis-related proteins. Collectively, we identified a new exosomes-mediated molecular mechanism by which CC cells transferred TUG1 via exosomes to recipient HUVECs, thus promoting angiogenesis, providing a promising target for early diagnosis of CC.

越来越多的证据表明，外泌体可以通过转移各种分子物质（包括长的非编码RNA（lncRNA））来介导人类癌变过程中的细胞间通讯。牛磺酸上调的1（TUG1）以前被报道为通过促进细胞增殖和其他重要的生物学行为而在宫颈癌（CC）中成为致癌lncRNA。然而，外泌体中TUG1的存在以及CC中外泌体TUG1的功能调节仍然难以捉摸。当前的研究针对外泌体介导的CC细胞系和内皮细胞之间的通讯，以及CC细胞和外泌体TUG1衍生的外泌体在影响血管生成中的作用。最初，发现在CC细胞及其分泌的外泌体中TUG1表达均被上调。TUG1以外泌体的方式从CC细胞转移到受体人脐静脉内皮细胞（HUVEC）。有趣的是，TUG1耗竭通过调节某些关键的血管生成相关基因，损害了外泌体介导的HUVEC的促血管生成潜力。此外，外体TUG1通过抑制caspase-3活性并影响凋亡相关蛋白而促进HUVEC的增殖。我们共同确定了新的外泌体介导的分子机制，CC细胞通过这种机制将TUG1通过外泌体转移至受体HUVEC，从而促进血管生成，为CC的早期诊断提供了有希望的靶标。此外，外体TUG1通过抑制caspase-3活性并影响凋亡相关蛋白而促进HUVEC的增殖。我们共同确定了新的外泌体介导的分子机制，CC细胞通过这种机制将TUG1通过外泌体转移至受体HUVEC，从而促进血管生成，为CC的早期诊断提供了有希望的靶标。此外，外体TUG1通过抑制caspase-3活性并影响凋亡相关蛋白而促进HUVEC的增殖。我们共同确定了新的外来体介导的分子机制，CC细胞通过该机制将TUG1通过外来体转移至受体HUVEC，从而促进血管生成，为CC的早期诊断提供了有希望的靶标。