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A549 细胞来源的外泌体通过 let-7c-5p 和 miR-181b-5p 诱导 BEAS-2B 细胞迁移、侵袭和 EMT。

Exosomes of A549 Cells Induced Migration, Invasion, and EMT of BEAS-2B Cells Related to let-7c-5p and miR-181b-5p.

机构信息

Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.

School of Medicine, Shanxi Datong University, Datong, China.

出版信息

Front Endocrinol (Lausanne). 2022 Jul 8;13:926769. doi: 10.3389/fendo.2022.926769. eCollection 2022.

Abstract

As carriers containing abundant biological information, exosomes could deliver the property of donor cells to recipient cells. Emerging studies have shown that tumor cells could secrete a mass of exosomes into the microenvironment to regulate bystander cells. However, the underlying mechanisms of such a phenomenon remain largely unexplored. In this research, we purified and identified the exosomes of A549 cells and found that A549-cell-derived exosomes promoted BEAS-2B cells migration, invasion, and epithelial-mesenchymal transition (EMT). Importantly, we observed that let-7c-5p and miR-181b-5p were attenuated in A549-cell-derived exosomes compared to BEAS-2B-cell-derived exosomes. The analysis of miRNA expression level in BEAS-2B cells indicated that incubation with A549-cell-derived exosomes reduced the expression levels of let-7c-5p and miR-181b-5p. In transient transfections assay, we found that downregulation of let-7c-5p and miR-181b-5p simultaneously showed stronger promotion of BEAS-2B cells migration and invasion than individually. Moreover, exosomes secreted from A549 cells with upregulated expression of let-7c-5p and miR-181b-5p significantly reduce their regulatory effect on BEAS-2B cells. Bioinformatics analyses revealed that let-7c-5p and miR-181b-5p inhibit the EMT process mainly by regulating focal adhesion and mitogen-activated protein kinase (MAPK) signaling pathway. Thus, our data demonstrated that A549-cell-derived exosomal let-7c-5p and miR-181b-5p could induce migration, invasion, and EMT in BEAS-2B cells, which might be regulated through focal adhesion and MAPK signaling pathway. The expression level of let-7c-5p and miR-181b-5p may show great significance for the early diagnosis of lung cancer.

摘要

作为富含生物信息的载体,外泌体可以将供体细胞的特性传递给受体细胞。新兴研究表明,肿瘤细胞可以将大量外泌体分泌到微环境中,以调节旁观者细胞。然而,这种现象的潜在机制在很大程度上仍未得到探索。在这项研究中,我们纯化并鉴定了 A549 细胞的外泌体,发现 A549 细胞衍生的外泌体促进了 BEAS-2B 细胞的迁移、侵袭和上皮-间充质转化(EMT)。重要的是,我们观察到 A549 细胞衍生的外泌体中的 let-7c-5p 和 miR-181b-5p 水平较 BEAS-2B 细胞衍生的外泌体减弱。对 BEAS-2B 细胞中 miRNA 表达水平的分析表明,用 A549 细胞衍生的外泌体孵育会降低 let-7c-5p 和 miR-181b-5p 的表达水平。在瞬时转染实验中,我们发现同时下调 let-7c-5p 和 miR-181b-5p 的表达比单独下调时更能显著促进 BEAS-2B 细胞的迁移和侵袭。此外,上调 let-7c-5p 和 miR-181b-5p 表达的 A549 细胞分泌的外泌体显著降低了它们对 BEAS-2B 细胞的调节作用。生物信息学分析表明,let-7c-5p 和 miR-181b-5p 主要通过调节粘着斑和丝裂原激活蛋白激酶(MAPK)信号通路来抑制 EMT 过程。因此,我们的数据表明,A549 细胞衍生的外泌体 let-7c-5p 和 miR-181b-5p 可以诱导 BEAS-2B 细胞的迁移、侵袭和 EMT,这可能通过粘着斑和 MAPK 信号通路进行调节。let-7c-5p 和 miR-181b-5p 的表达水平可能对肺癌的早期诊断具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4210/9309177/9b4ae064e786/fendo-13-926769-g001.jpg

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