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Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line

Chronic inflammation is associated with cancer. CXCL8 promotes tumor microenvironment construction through recruiting leukocytes and endothelial progenitor cells that are involved in angiogenesis. It also enhances tumor cell proliferation and migration. Metformin, type II diabetes medication, demons...

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Detalles Bibliográficos
Autores principales: Xiao, Zhihui, Wu, Wenjun, Poltoratsky, Vladimir
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5632916/
https://www.ncbi.nlm.nih.gov/pubmed/29147073
http://dx.doi.org/10.1155/2017/6589423
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author Xiao, Zhihui
Wu, Wenjun
Poltoratsky, Vladimir
author_facet Xiao, Zhihui
Wu, Wenjun
Poltoratsky, Vladimir
author_sort Xiao, Zhihui
collection PubMed
description Chronic inflammation is associated with cancer. CXCL8 promotes tumor microenvironment construction through recruiting leukocytes and endothelial progenitor cells that are involved in angiogenesis. It also enhances tumor cell proliferation and migration. Metformin, type II diabetes medication, demonstrates anticancer properties via suppressing inflammation, tumor cell proliferation, angiogenesis, and metastasis. This study intended to address the role of metformin in regulation of CXCL8 expression and cell proliferation and migration. Our data indicated that metformin suppressed LPS-induced CXCL8 expression in a dose-dependent manner through inhibiting NF-κB, but not AP-1 and C/EBP, activities under the conditions we used. This inhibitory effect of metformin is achieved through dampening LPS-induced NF-κB nuclear translocation. Cell migration was inhibited by metformin under high dose (10 mM), but not cell proliferation.
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spelling pubmed-56329162017-11-16 Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line Xiao, Zhihui Wu, Wenjun Poltoratsky, Vladimir Mediators Inflamm Research Article Chronic inflammation is associated with cancer. CXCL8 promotes tumor microenvironment construction through recruiting leukocytes and endothelial progenitor cells that are involved in angiogenesis. It also enhances tumor cell proliferation and migration. Metformin, type II diabetes medication, demonstrates anticancer properties via suppressing inflammation, tumor cell proliferation, angiogenesis, and metastasis. This study intended to address the role of metformin in regulation of CXCL8 expression and cell proliferation and migration. Our data indicated that metformin suppressed LPS-induced CXCL8 expression in a dose-dependent manner through inhibiting NF-κB, but not AP-1 and C/EBP, activities under the conditions we used. This inhibitory effect of metformin is achieved through dampening LPS-induced NF-κB nuclear translocation. Cell migration was inhibited by metformin under high dose (10 mM), but not cell proliferation. Hindawi 2017 2017-09-24 /pmc/articles/PMC5632916/ /pubmed/29147073 http://dx.doi.org/10.1155/2017/6589423 Text en Copyright © 2017 Zhihui Xiao et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Xiao, Zhihui
Wu, Wenjun
Poltoratsky, Vladimir
Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line
title Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line
title_full Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line
title_fullStr Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line
title_full_unstemmed Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line
title_short Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line
title_sort metformin suppressed cxcl8 expression and cell migration in hek293/tlr4 cell line
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5632916/
https://www.ncbi.nlm.nih.gov/pubmed/29147073
http://dx.doi.org/10.1155/2017/6589423
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