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微小 RNA-631 来源于骨髓间充质干细胞外泌体，通过调节 E2F 转录因子家族 2/磷脂酰肌醇 3-激酶/ Akt 信号通路促进非小细胞肺癌的恶性行为。

MicroRNA-631 deriving from bone marrow mesenchymal stem cell exosomes facilitates the malignant behavior of non-small cell lung cancer via modulating the E2F family of transcription factor 2/phosphatidylinositol 3-kinase/Akt signaling pathway.

机构信息

Department of Pulmonary and Critical Care Medicine, Taicang Hospital of Chinese Medicine, Taicang City, Jiangsu Province, China.

Department of Pulmonary and Critical Care Medicine, Jiangsu Province Hospital of Chinese Medince, Nanjing, Jiangsu Province, China.

出版信息

Bioengineered. 2022 Apr;13(4):8382-8395. doi: 10.1080/21655979.2022.2036891.

DOI:10.1080/21655979.2022.2036891
PMID:35353027
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9161988/
Abstract

The exosomes (Exo) had always been considered as transport vectors for microRNA (miRNA). An increasing number of data had clarified the influence of Exo on the cell progression of non-small cell lung cancer (NSCLC). Nevertheless, its specific mechanism had not yet been verified. This work was to explore the potential mechanism of Exo-derived miR-631 targeting and regulating E2F family of transcription factor 2 (E2F2) to repress the malignant behavior of NSCLC cells. Test of microRNA (miR)-631 and E2F2 in NSCLC was performed. BMSCs-Exo that altered miR-631 was co-cultured with NSCLC cells. Detection of the cloning and progression of NSCLC cells was performed. Testification of the targeting of miR-631 with E2F2 was conducted. In experiments were performed to verify the results in . In short, elevation of miR-631 Exo repressed the advancement and phosphatidylinositol 3-kinase/Akt activation of NSCLC cells, while silence of miR-631 was in the opposite. In terms of mechanism, miR-631 exerted the influence via targeting E2F2. The coincident results were obtained in animal models. In brief, BMSC-Exo mediated E2F2 via delivering miR-631 to NSCLC cells to modulate the malignant behavior of NSCLC.

摘要

外泌体 (Exo) 一直被认为是 microRNA (miRNA) 的运输载体。越来越多的数据阐明了外泌体对非小细胞肺癌 (NSCLC) 细胞进展的影响。然而，其具体机制尚未得到验证。本研究旨在探讨外泌体衍生的 miR-631 靶向和调节转录因子 E2F 家族 2 (E2F2) 的潜在机制，以抑制 NSCLC 细胞的恶性行为。检测 NSCLC 中的 miR-631 和 E2F2。改变 miR-631 的 BMSCs-Exo 与 NSCLC 细胞共培养。检测 NSCLC 细胞的克隆和进展。进行 miR-631 与 E2F2 的靶向检测。在 中进行实验以验证 的结果。简而言之，miR-631 Exo 的升高抑制了 NSCLC 细胞的进展和磷脂酰肌醇 3-激酶/ Akt 激活，而 miR-631 的沉默则相反。就机制而言，miR-631 通过靶向 E2F2 发挥作用。在动物模型中也得到了一致的结果。总之，BMSC-Exo 通过向 NSCLC 细胞传递 miR-631 来介导 E2F2，从而调节 NSCLC 的恶性行为。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/462ad48a5645/KBIE_A_2036891_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/a590f4d42da8/KBIE_A_2036891_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/da826bc90eac/KBIE_A_2036891_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/3d4d79e6f0fd/KBIE_A_2036891_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/be720b3d16bc/KBIE_A_2036891_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/0b6621085b47/KBIE_A_2036891_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/02f751b8bc51/KBIE_A_2036891_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/b068a2b367ce/KBIE_A_2036891_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/462ad48a5645/KBIE_A_2036891_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/a590f4d42da8/KBIE_A_2036891_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/da826bc90eac/KBIE_A_2036891_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/3d4d79e6f0fd/KBIE_A_2036891_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/be720b3d16bc/KBIE_A_2036891_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/0b6621085b47/KBIE_A_2036891_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/02f751b8bc51/KBIE_A_2036891_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/b068a2b367ce/KBIE_A_2036891_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b8/9161988/462ad48a5645/KBIE_A_2036891_F0007_OC.jpg

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