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

BACKGROUND AND OBJECTIVE: 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 ef...

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Detalles Bibliográficos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 中国肺癌杂志编辑部 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9845090/
https://www.ncbi.nlm.nih.gov/pubmed/36617469
http://dx.doi.org/10.3779/j.issn.1009-3419.2022.101.50
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collection PubMed
description BACKGROUND AND OBJECTIVE: 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. CONCLUSION: Tumor cell-derived exosome miR-10b promotes A549 cell invasion and EMT through M2 macrophage polarization.
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spelling pubmed-98450902023-01-30 外泌体miR-10b通过调控巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮间质转化 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: 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. CONCLUSION: Tumor cell-derived exosome miR-10b promotes A549 cell invasion and EMT through M2 macrophage polarization. 中国肺癌杂志编辑部 2022-12-20 /pmc/articles/PMC9845090/ /pubmed/36617469 http://dx.doi.org/10.3779/j.issn.1009-3419.2022.101.50 Text en 版权所有©《中国肺癌杂志》编辑部2022 https://creativecommons.org/licenses/by/3.0/This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/.
spellingShingle 基础研究
外泌体miR-10b通过调控巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮间质转化
title 外泌体miR-10b通过调控巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮间质转化
title_full 外泌体miR-10b通过调控巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮间质转化
title_fullStr 外泌体miR-10b通过调控巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮间质转化
title_full_unstemmed 外泌体miR-10b通过调控巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮间质转化
title_short 外泌体miR-10b通过调控巨噬细胞M2极化促进肺腺癌A549细胞的侵袭和上皮间质转化
title_sort 外泌体mir-10b通过调控巨噬细胞m2极化促进肺腺癌a549细胞的侵袭和上皮间质转化
topic 基础研究
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9845090/
https://www.ncbi.nlm.nih.gov/pubmed/36617469
http://dx.doi.org/10.3779/j.issn.1009-3419.2022.101.50
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