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The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation

Recent studies have demonstrated a relationship between oral bacteria and systemic inflammation. Endothelial cells (ECs), which line blood vessels, control the opening and closing of the vascular barrier and contribute to hematogenous metastasis; however, the role of oral bacteria‐induced vascular i...

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Autores principales: Yu, Li, Maishi, Nako, Akahori, Erika, Hasebe, Akira, Takeda, Ryo, Matsuda, Aya Yanagawa, Hida, Yasuhiro, Nam, Jin‐Min, Onodera, Yasuhito, Kitagawa, Yoshimasa, Hida, Kyoko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9633306/
https://www.ncbi.nlm.nih.gov/pubmed/35997541
http://dx.doi.org/10.1111/cas.15538
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author Yu, Li
Maishi, Nako
Akahori, Erika
Hasebe, Akira
Takeda, Ryo
Matsuda, Aya Yanagawa
Hida, Yasuhiro
Nam, Jin‐Min
Onodera, Yasuhito
Kitagawa, Yoshimasa
Hida, Kyoko
author_facet Yu, Li
Maishi, Nako
Akahori, Erika
Hasebe, Akira
Takeda, Ryo
Matsuda, Aya Yanagawa
Hida, Yasuhiro
Nam, Jin‐Min
Onodera, Yasuhito
Kitagawa, Yoshimasa
Hida, Kyoko
author_sort Yu, Li
collection PubMed
description Recent studies have demonstrated a relationship between oral bacteria and systemic inflammation. Endothelial cells (ECs), which line blood vessels, control the opening and closing of the vascular barrier and contribute to hematogenous metastasis; however, the role of oral bacteria‐induced vascular inflammation in tumor metastasis remains unclear. In this study, we examined the phenotypic changes in vascular ECs following Streptococcus mutans (S. mutans) stimulation in vitro and in vivo. The expression of molecules associated with vascular inflammation and barrier‐associated adhesion was analyzed. Tumor metastasis was evaluated after intravenous injection of S. mutans in murine breast cancer hematogenous metastasis model. The results indicated that S. mutans invaded the ECs accompanied by inflammation and NF‐κB activation. S. mutans exposure potentially disrupts endothelial integrity by decreasing vascular endothelial (VE)‐cadherin expression. The migration and adhesion of tumor cells were enhanced in S. mutans‐stimulated ECs. Furthermore, S. mutans‐induced lung vascular inflammation promoted breast cancer cell metastasis to the lungs in vivo. The results indicate that oral bacteria promote tumor metastasis through vascular inflammation and the disruption of vascular barrier function. Improving oral hygiene in patients with cancer is of great significance in preventing postoperative pneumonia and tumor metastasis.
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spelling pubmed-96333062022-11-07 The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation Yu, Li Maishi, Nako Akahori, Erika Hasebe, Akira Takeda, Ryo Matsuda, Aya Yanagawa Hida, Yasuhiro Nam, Jin‐Min Onodera, Yasuhito Kitagawa, Yoshimasa Hida, Kyoko Cancer Sci Original Articles Recent studies have demonstrated a relationship between oral bacteria and systemic inflammation. Endothelial cells (ECs), which line blood vessels, control the opening and closing of the vascular barrier and contribute to hematogenous metastasis; however, the role of oral bacteria‐induced vascular inflammation in tumor metastasis remains unclear. In this study, we examined the phenotypic changes in vascular ECs following Streptococcus mutans (S. mutans) stimulation in vitro and in vivo. The expression of molecules associated with vascular inflammation and barrier‐associated adhesion was analyzed. Tumor metastasis was evaluated after intravenous injection of S. mutans in murine breast cancer hematogenous metastasis model. The results indicated that S. mutans invaded the ECs accompanied by inflammation and NF‐κB activation. S. mutans exposure potentially disrupts endothelial integrity by decreasing vascular endothelial (VE)‐cadherin expression. The migration and adhesion of tumor cells were enhanced in S. mutans‐stimulated ECs. Furthermore, S. mutans‐induced lung vascular inflammation promoted breast cancer cell metastasis to the lungs in vivo. The results indicate that oral bacteria promote tumor metastasis through vascular inflammation and the disruption of vascular barrier function. Improving oral hygiene in patients with cancer is of great significance in preventing postoperative pneumonia and tumor metastasis. John Wiley and Sons Inc. 2022-09-12 2022-11 /pmc/articles/PMC9633306/ /pubmed/35997541 http://dx.doi.org/10.1111/cas.15538 Text en © 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Articles
Yu, Li
Maishi, Nako
Akahori, Erika
Hasebe, Akira
Takeda, Ryo
Matsuda, Aya Yanagawa
Hida, Yasuhiro
Nam, Jin‐Min
Onodera, Yasuhito
Kitagawa, Yoshimasa
Hida, Kyoko
The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation
title The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation
title_full The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation
title_fullStr The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation
title_full_unstemmed The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation
title_short The oral bacterium Streptococcus mutans promotes tumor metastasis by inducing vascular inflammation
title_sort oral bacterium streptococcus mutans promotes tumor metastasis by inducing vascular inflammation
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9633306/
https://www.ncbi.nlm.nih.gov/pubmed/35997541
http://dx.doi.org/10.1111/cas.15538
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