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[外泌体miR-10b通过调节巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮-间质转化]

[Exosomal miR-10b Promotes Invasion and Epithelial-mesenchymal Transformation of Lung Adenocarcinoma A549 Cells by Regulating Macrophage M2 Polarization].

作者信息

Yuan Yan, Guo Limin, Guo Shan

机构信息

Xinxiang Central Hospital, Xinxiang 453000, China.

出版信息

Zhongguo Fei Ai Za Zhi. 2022 Dec 20;25(12):835-842. doi: 10.3779/j.issn.1009-3419.2022.101.50.

Abstract

BACKGROUND

Metastasis is the main cause of death in patients with lung cancer. Macrophages are innate immune cells that play important roles in cancer metastasis. Exosomes could play an important role of communication between tumor cells and macrophages. This study investigated the effect of miR-10b on cell growth invasion and epithelial mesenchymal transition (EMT) in lung adenocarcinoma A549 cell exosomes.

METHODS

Exosomes were isolated from A549 cells and identified by transmission electron microscopy (TEM) and Western blot. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis. Cell migration and invasion were detected by Transwell assay. The expression of mRNA and protein were assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot, respectively.

RESULTS

The expression of miR-10b was up-regulated in non-small cell lung cancer, and miR-10b inhibitor could inhibit the proliferation of A549 cell. Meanwhile, the tumor cell-derived exosome miR-10b promoted the invasion of A549 cell and EMT by promoting the M2 polarization of macrophages.

CONCLUSIONS

Tumor cell-derived exosome miR-10b promotes A549 cell invasion and EMT through M2 macrophage polarization.

摘要

背景

转移是肺癌患者死亡的主要原因。巨噬细胞是先天性免疫细胞,在癌症转移中起重要作用。外泌体可能在肿瘤细胞与巨噬细胞之间的通讯中发挥重要作用。本研究调查了miR-10b对肺腺癌A549细胞外泌体中细胞生长、侵袭及上皮-间质转化(EMT)的影响。

方法

从A549细胞中分离外泌体,并通过透射电子显微镜(TEM)和蛋白质免疫印迹法进行鉴定。采用CCK-8法和流式细胞术检测细胞增殖和凋亡。通过Transwell实验检测细胞迁移和侵袭。分别采用定量逆转录聚合酶链反应(RT-qPCR)和蛋白质免疫印迹法评估mRNA和蛋白质的表达。

结果

miR-10b在非小细胞肺癌中表达上调,miR-10b抑制剂可抑制A549细胞增殖。同时,肿瘤细胞来源的外泌体miR-10b通过促进巨噬细胞的M2极化促进A549细胞侵袭和EMT。

结论

肿瘤细胞来源的外泌体miR-10b通过M2巨噬细胞极化促进A549细胞侵袭和EMT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b798/9845090/d1df8860d2b8/zgfazz-25-12-835-1.jpg

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