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IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages
PURPOSE: Non-small cell lung cancer (NSCLC) is currently a problem in the clinic and in society. Tumor-related macrophages (TAMs) in the tumor microenvironment (TME) play a vital role in the development of NSCLC. PATIENTS AND METHODS: Bioinformatics was used to analyze the role of Indoleamine 2,3-di...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10178912/ https://www.ncbi.nlm.nih.gov/pubmed/37187591 http://dx.doi.org/10.2147/IJGM.S398908 |
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author | Chen, Xiao Yao, Jie Zhang, Meng-Yu Li, Rui Liu, Xiao Qu, Yi-Qing |
author_facet | Chen, Xiao Yao, Jie Zhang, Meng-Yu Li, Rui Liu, Xiao Qu, Yi-Qing |
author_sort | Chen, Xiao |
collection | PubMed |
description | PURPOSE: Non-small cell lung cancer (NSCLC) is currently a problem in the clinic and in society. Tumor-related macrophages (TAMs) in the tumor microenvironment (TME) play a vital role in the development of NSCLC. PATIENTS AND METHODS: Bioinformatics was used to analyze the role of Indoleamine 2,3-dioxygenase 1 (IDO1) in NSCLC and the correlation of its expression with CD163 expression. The expression of CD163 and IDO1 was measured by immunohistochemistry, and their colocalization was assessed by immunofluorescence. M2 macrophage polarization was induced, and a coculture model of NSCLC cells and macrophages was established. RESULTS: Bioinformatics analysis showed that IDO1 promoted the metastasis and differentiation of NSCLC and inhibited DNA repair. Moreover, the expression of IDO1 was positively correlated with CD163 expression. We discovered that IDO1 expression was related to M2 macrophage differentiation. In vitro, we showed that increased IDO1 expression promoted the invasion, proliferation, and metastasis of NSCLC cells. CONCLUSION: In conclusion, we determined that IDO1 can regulate the M2 polarization of TAMs and promote the progression of NSCLC, which provides partial theoretical evidence for the use of IDO1 inhibitors in the treatment of NSCLC. |
format | Online Article Text |
id | pubmed-10178912 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-101789122023-05-13 IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages Chen, Xiao Yao, Jie Zhang, Meng-Yu Li, Rui Liu, Xiao Qu, Yi-Qing Int J Gen Med Original Research PURPOSE: Non-small cell lung cancer (NSCLC) is currently a problem in the clinic and in society. Tumor-related macrophages (TAMs) in the tumor microenvironment (TME) play a vital role in the development of NSCLC. PATIENTS AND METHODS: Bioinformatics was used to analyze the role of Indoleamine 2,3-dioxygenase 1 (IDO1) in NSCLC and the correlation of its expression with CD163 expression. The expression of CD163 and IDO1 was measured by immunohistochemistry, and their colocalization was assessed by immunofluorescence. M2 macrophage polarization was induced, and a coculture model of NSCLC cells and macrophages was established. RESULTS: Bioinformatics analysis showed that IDO1 promoted the metastasis and differentiation of NSCLC and inhibited DNA repair. Moreover, the expression of IDO1 was positively correlated with CD163 expression. We discovered that IDO1 expression was related to M2 macrophage differentiation. In vitro, we showed that increased IDO1 expression promoted the invasion, proliferation, and metastasis of NSCLC cells. CONCLUSION: In conclusion, we determined that IDO1 can regulate the M2 polarization of TAMs and promote the progression of NSCLC, which provides partial theoretical evidence for the use of IDO1 inhibitors in the treatment of NSCLC. Dove 2023-05-08 /pmc/articles/PMC10178912/ /pubmed/37187591 http://dx.doi.org/10.2147/IJGM.S398908 Text en © 2023 Chen et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Chen, Xiao Yao, Jie Zhang, Meng-Yu Li, Rui Liu, Xiao Qu, Yi-Qing IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages |
title | IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages |
title_full | IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages |
title_fullStr | IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages |
title_full_unstemmed | IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages |
title_short | IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages |
title_sort | ido1 promotes the progression of nsclc by regulating the polarization of m2 macrophages |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10178912/ https://www.ncbi.nlm.nih.gov/pubmed/37187591 http://dx.doi.org/10.2147/IJGM.S398908 |
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