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缺氧胶质瘤衍生的外泌体将 miR-1246 和 miR-10b-5p 递送至正常氧胶质瘤细胞,促进迁移和侵袭。

Exosomes derived from hypoxic glioma deliver miR-1246 and miR-10b-5p to normoxic glioma cells to promote migration and invasion.

机构信息

Department of Neurosurgery, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, China.

Shandong Key Laboratory of Brain Function Remodeling, Jinan, 250012, Shandong, China.

出版信息

Lab Invest. 2021 May;101(5):612-624. doi: 10.1038/s41374-020-00522-0. Epub 2021 Jan 14.

Abstract

Hypoxia is an important feature of the tumor microenvironment and is associated with glioma progression and patient outcome. Exosomes have been implicated in the intercellular communication in the tumor microenvironment. However, the effects of hypoxic glioma exosomes on glioma migration and invasion and the underlying mechanisms remain poorly understood. In this study, we found that exosomes derived from hypoxic glioma cells (H-GDEs) promoted normoxic glioma migration and invasion in vitro and in vivo. Given that exosomes can regulate recipient cell functions by delivering microRNAs, we further revealed miR-1246 and miR-10b-5p were upregulated significantly in H-GDEs and delivered to normoxic glioma cells by H-GDEs. Moreover, we determined the clinical relevance of miR-1246 and miR-10b-5p in glioma patients. Subsequent investigations indicated that miR-1246 and miR-10b-5p markedly induced glioma migration and invasion in vitro and in vivo. Finally, we demonstrated that miR-1246 and miR-10b-5p induced glioma migration and invasion by directly targeting FRK and TFAP2A respectively. In conclusion, our findings suggest that the hypoxic microenvironment stimulates glioma to generate miR-1246- and miR-10b-5p-rich exosomes that are delivered to normoxic glioma cells to promote their migration and invasion; treatment targeting miR-1246 and miR-10b-5p may impair the motility of gliomas, providing a novel direction for the development of antitumor therapy.

摘要

缺氧是肿瘤微环境的一个重要特征,与胶质瘤的进展和患者预后相关。外泌体参与了肿瘤微环境中的细胞间通讯。然而,缺氧胶质瘤来源的外泌体(H-GDEs)对胶质瘤迁移和侵袭的影响及其潜在机制仍知之甚少。在本研究中,我们发现缺氧胶质瘤细胞来源的外泌体(H-GDEs)促进了体外和体内正常氧合胶质瘤的迁移和侵袭。鉴于外泌体可以通过传递 microRNAs 来调节受体细胞的功能,我们进一步揭示了 H-GDEs 中 miR-1246 和 miR-10b-5p 显著上调,并通过 H-GDEs 递送到正常氧合胶质瘤细胞。此外,我们确定了 miR-1246 和 miR-10b-5p 在胶质瘤患者中的临床相关性。随后的研究表明,miR-1246 和 miR-10b-5p 在体外和体内显著诱导了胶质瘤的迁移和侵袭。最后,我们证明了 miR-1246 和 miR-10b-5p 通过直接靶向 FRK 和 TFAP2A 分别诱导了胶质瘤的迁移和侵袭。总之,我们的研究结果表明,缺氧微环境刺激胶质瘤产生富含 miR-1246 和 miR-10b-5p 的外泌体,递送到正常氧合的胶质瘤细胞中,促进其迁移和侵袭;针对 miR-1246 和 miR-10b-5p 的治疗可能会削弱胶质瘤的运动能力,为抗肿瘤治疗的发展提供了新的方向。

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