The role of Fusobacterium nucleatum in colorectal cancer: from carcinogenesis to clinical management
Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis...
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Abstract | Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum-associated CRC. |
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AbstractList | Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of
Fusobacterium nucleatum
(
F. nucleatum
) in colorectal carcinoma tissue; many studies have indicated that
F. nucleatum
is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of
F. nucleatum
promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore,
F. nucleatum
recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression.
F. nucleatum
was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition,
F. nucleatum
increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable
F. nucleatum
was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of
F. nucleatum
in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with
F. nucleatum
-associated CRC. Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor‐infiltrating immune cells, thus yielding a pro‐inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll‐like receptor 2 (TLR2)/toll‐like receptor 4 (TLR4) signaling and microRNA (miRNA)‐21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA‐18a*, miRNA‐4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum‐associated CRC. Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying mo-lecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum-associated CRC. Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum-associated CRC. Keywords: Fusobacterium nucleatum, Colorectal carcinoma, Carcinogenesis, Immune microenvironment, Intervention therapy Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum-associated CRC.Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum-associated CRC. Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of ( ) in colorectal carcinoma tissue; many studies have indicated that is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with -associated CRC. |
Author | Sun, Chun-Hui Wang, Bo Zhang, Xiao-Ying Wang, Xin-Cheng Qiu, Miao-Juan Zhao, Jing Li, Bin-Bin Tang, Di Li, Wen-Bing Li, Ting-Ting Zhu, Cheng-Ming Qian, Zhi-Rong |
AuthorAffiliation | Equipe Communication Intercellulaire et Infections Microbiennes,Centre de Recherche Interdisciplinaire en Biologie (CIRB),Collège de France,Paris 75005,France;Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China;School of Biological Sciences,Nanyang Technological University,Singapore 637551,Singapore%Department of Oncology,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Health Management Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Department of Gastroenterology,The Second Medical Center of Chinese PLA General Hospital,Beijing 100853,China%Department of Pathology,National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital,Ch |
AuthorAffiliation_xml | – name: Equipe Communication Intercellulaire et Infections Microbiennes,Centre de Recherche Interdisciplinaire en Biologie (CIRB),Collège de France,Paris 75005,France;Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China;School of Biological Sciences,Nanyang Technological University,Singapore 637551,Singapore%Department of Oncology,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Health Management Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Department of Gastroenterology,The Second Medical Center of Chinese PLA General Hospital,Beijing 100853,China%Department of Pathology,National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital,Chinese Academy of Medical Sciences,Peking Union Medical College,Beijing 100021,China%Department of General Surgery,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China – name: g Department of Pathology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100021, China – name: d Department of Oncology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – name: e Health Management Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – name: f Department of Gastroenterology, The Second Medical Center of Chinese PLA General Hospital, Beijing 100853, China – name: h Department of General Surgery, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – name: a Equipe Communication Intercellulaire et Infections Microbiennes, Centre de Recherche Interdisciplinaire en Biologie (CIRB), Collège de France, Paris 75005, France – name: c School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore – name: b Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China |
Author_xml | – sequence: 1 givenname: Chun-Hui surname: Sun fullname: Sun, Chun-Hui organization: Equipe Communication Intercellulaire et Infections Microbiennes, Centre de Recherche Interdisciplinaire en Biologie (CIRB), Collège de France, Paris 75005, France – sequence: 2 givenname: Bin-Bin surname: Li fullname: Li, Bin-Bin organization: Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 3 givenname: Bo surname: Wang fullname: Wang, Bo organization: Department of Oncology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 4 givenname: Jing surname: Zhao fullname: Zhao, Jing organization: Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 5 givenname: Xiao-Ying surname: Zhang fullname: Zhang, Xiao-Ying organization: Health Management Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 6 givenname: Ting-Ting surname: Li fullname: Li, Ting-Ting organization: Department of Gastroenterology, The Second Medical Center of Chinese PLA General Hospital, Beijing 100853, China – sequence: 7 givenname: Wen-Bing surname: Li fullname: Li, Wen-Bing organization: Department of Pathology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100021, China – sequence: 8 givenname: Di surname: Tang fullname: Tang, Di organization: Department of General Surgery, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 9 givenname: Miao-Juan surname: Qiu fullname: Qiu, Miao-Juan organization: Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 10 givenname: Xin-Cheng surname: Wang fullname: Wang, Xin-Cheng organization: Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 11 givenname: Cheng-Ming surname: Zhu fullname: Zhu, Cheng-Ming organization: Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China – sequence: 12 givenname: Zhi-Rong surname: Qian fullname: Qian, Zhi-Rong email: qianzhir@mail.sysu.edu.cn organization: Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31891129$$D View this record in MEDLINE/PubMed |
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Keywords | Immune microenvironment Intervention therapy Fusobacterium nucleatum Carcinogenesis Colorectal carcinoma |
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PublicationDate | September 2019 |
PublicationDateYYYYMMDD | 2019-09-01 |
PublicationDate_xml | – month: 09 year: 2019 text: September 2019 |
PublicationDecade | 2010 |
PublicationPlace | China |
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PublicationTitle | Chronic diseases and translational medicine |
PublicationTitleAlternate | Chronic Dis Transl Med |
PublicationTitle_FL | Chronic Diseases and Translational Medicine |
PublicationYear | 2019 |
Publisher | Elsevier B.V Equipe Communication Intercellulaire et Infections Microbiennes,Centre de Recherche Interdisciplinaire en Biologie (CIRB),Collège de France,Paris 75005,France Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China School of Biological Sciences,Nanyang Technological University,Singapore 637551,Singapore%Department of Oncology,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Health Management Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Department of Gastroenterology,The Second Medical Center of Chinese PLA General Hospital,Beijing 100853,China%Department of Pathology,National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital,Chinese Academy of Medical Sciences,Peking Union Medical College,Beijing 100021,China%Department of General Surgery,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China Chinese Medical Association Wiley |
Publisher_xml | – name: Elsevier B.V – name: School of Biological Sciences,Nanyang Technological University,Singapore 637551,Singapore%Department of Oncology,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Health Management Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Department of Gastroenterology,The Second Medical Center of Chinese PLA General Hospital,Beijing 100853,China%Department of Pathology,National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital,Chinese Academy of Medical Sciences,Peking Union Medical College,Beijing 100021,China%Department of General Surgery,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China – name: Equipe Communication Intercellulaire et Infections Microbiennes,Centre de Recherche Interdisciplinaire en Biologie (CIRB),Collège de France,Paris 75005,France – name: Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China%Research Center,The Seventh Affiliated Hospital,Sun Yat-sen University,Shenzhen,Guangdong 518107,China – name: Chinese Medical Association – name: Wiley |
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Snippet | Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F.... Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (... Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of ( ) in colorectal carcinoma... |
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SubjectTerms | Carcinogenesis Colorectal carcinoma Fusobacterium nucleatum Immune microenvironment Intervention therapy |
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Title | The role of Fusobacterium nucleatum in colorectal cancer: from carcinogenesis to clinical management |
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