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Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse Model of Bladder Cancer
Background: Lentinan (LNT), an isolated traditional Chinese herbal component, has antitumor potential. In the current study, the intrinsic mechanism of LNT-induced immunity against bladder cancer was explored in a mouse model. Methods: In the mouse model of bladder cancer, we used flow cytometry to...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7401035/ https://www.ncbi.nlm.nih.gov/pubmed/32735179 http://dx.doi.org/10.1177/1534735420946823 |
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author | Sun, Ming Bu, Renge Zhang, Bin Cao, Yaming Liu, Chengyang Zhao, Wenyan |
author_facet | Sun, Ming Bu, Renge Zhang, Bin Cao, Yaming Liu, Chengyang Zhao, Wenyan |
author_sort | Sun, Ming |
collection | PubMed |
description | Background: Lentinan (LNT), an isolated traditional Chinese herbal component, has antitumor potential. In the current study, the intrinsic mechanism of LNT-induced immunity against bladder cancer was explored in a mouse model. Methods: In the mouse model of bladder cancer, we used flow cytometry to detect the LNT caused population changes of T cells, macrophages, MDSC cells, and Treg cells. ELISA was used to evaluate cytokines expression in the supernatant of splenocytes. Results: We found that the administration of LNT increased the proportions of CD3(+)CD4(+) and CD3(+)CD8(+) T cell subsets as well as CD11b(+)F480(+) macrophages, whereas it diminished the subpopulations of CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) and Gr-1(+)CD11b(+) myeloid-derived suppressor cells (MDSCs). LNT also upregulated the expression of interferon (IFN)-γ and interleukin (IL)-12, accompanied by a significant reduction in IL-10 and tumor growth factor (TGF)-β (P < .05). Our research further confirmed the synergy between LNT and gemcitabine (GEM) to activate immunity and inhibit the growth of bladder tumors in mouse model. Conclusions: LNT induced macrophage activation, followed by the enhanced proliferation of CD4(+) and CD8(+) T cells, and the upregulated expression of IFN-γ and IL-2. Meanwhile, the proportions of MDSCs and Tregs were downregulated, leading to a reduced expression of the anti-inflammatory cytokines IL-10 and TGF-β. The synergy between LNT and GEM provides additional evidence supporting the application of this traditional Chinese herbal component for bladder cancer therapy. |
format | Online Article Text |
id | pubmed-7401035 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-74010352020-08-10 Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse Model of Bladder Cancer Sun, Ming Bu, Renge Zhang, Bin Cao, Yaming Liu, Chengyang Zhao, Wenyan Integr Cancer Ther Research Article Background: Lentinan (LNT), an isolated traditional Chinese herbal component, has antitumor potential. In the current study, the intrinsic mechanism of LNT-induced immunity against bladder cancer was explored in a mouse model. Methods: In the mouse model of bladder cancer, we used flow cytometry to detect the LNT caused population changes of T cells, macrophages, MDSC cells, and Treg cells. ELISA was used to evaluate cytokines expression in the supernatant of splenocytes. Results: We found that the administration of LNT increased the proportions of CD3(+)CD4(+) and CD3(+)CD8(+) T cell subsets as well as CD11b(+)F480(+) macrophages, whereas it diminished the subpopulations of CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) and Gr-1(+)CD11b(+) myeloid-derived suppressor cells (MDSCs). LNT also upregulated the expression of interferon (IFN)-γ and interleukin (IL)-12, accompanied by a significant reduction in IL-10 and tumor growth factor (TGF)-β (P < .05). Our research further confirmed the synergy between LNT and gemcitabine (GEM) to activate immunity and inhibit the growth of bladder tumors in mouse model. Conclusions: LNT induced macrophage activation, followed by the enhanced proliferation of CD4(+) and CD8(+) T cells, and the upregulated expression of IFN-γ and IL-2. Meanwhile, the proportions of MDSCs and Tregs were downregulated, leading to a reduced expression of the anti-inflammatory cytokines IL-10 and TGF-β. The synergy between LNT and GEM provides additional evidence supporting the application of this traditional Chinese herbal component for bladder cancer therapy. SAGE Publications 2020-07-31 /pmc/articles/PMC7401035/ /pubmed/32735179 http://dx.doi.org/10.1177/1534735420946823 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Research Article Sun, Ming Bu, Renge Zhang, Bin Cao, Yaming Liu, Chengyang Zhao, Wenyan Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse Model of Bladder Cancer |
title | Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse
Model of Bladder Cancer |
title_full | Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse
Model of Bladder Cancer |
title_fullStr | Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse
Model of Bladder Cancer |
title_full_unstemmed | Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse
Model of Bladder Cancer |
title_short | Lentinan Inhibits Tumor Progression by Immunomodulation in a Mouse
Model of Bladder Cancer |
title_sort | lentinan inhibits tumor progression by immunomodulation in a mouse
model of bladder cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7401035/ https://www.ncbi.nlm.nih.gov/pubmed/32735179 http://dx.doi.org/10.1177/1534735420946823 |
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