<i>Porphyromonas gingivalis</i> Promotes Colorectal Carcinoma by Activating the Hematopoietic <i>NLRP3</i> Inflammasome

Wang, Xi; Jia, Yanming; Wen, Liling; Mu, Wenxin; Wu, Xianrui; Liu, Tao; Liu, Xiangqi; Fang, Juan; Luan, Yizhao; Chen, Ping; Gao, Jinlong; Nguyen, Ky-Anh; Cui, Jun; Zeng, Gucheng; Lan, Ping; Chen, Qianming; Cheng, Bin; Wang, Zhi

doi:10.1158/0008-5472.can-20-3827

Cited by 112 publications

(93 citation statements)

References 59 publications

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“…However, another oral anaerobe Porphyromonas gingivalis (P. gingivalis), which has been claimed to be correlated with certain cancers apart from being a well-documented periodontitis-related pathogen (35,36), did not have the similar impact on H3K27ac level (Fig. 5E).…”

Section: F Nucleatum Promotes Angptl4 Expression By Facilitating the H3k27acmentioning

confidence: 97%

ANGPTL4-Mediated Promotion of Glycolysis Facilitates the Colonization ofFusobacterium nucleatumin Colorectal Cancer

Zheng

Zhou

et al. 2021

Cancer Research

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Colorectal cancer (CRC) is a severe health problem worldwide, and accumulating evidence supports the contribution of Fusobacterium nucleatum to CRC development, metastasis, and chemoresistance. However, the mechanisms underlying the colonization of F. nucleatum in CRC tissue is not yet clarified. Here we demonstrate that F. nucleatum infection mediated elevation of angiopoietin-like 4 (ANGPTL4) expression. Upregulated ANGPTL4 promoted glucose uptake and glycolysis activity in CRC cells in vitro and in vivo, which are necessary for the colonization of F. nucleatum. Furthermore, overall increased acetylation of histone H3 lysine 27 was observed in F. nucleatum infected CRC cells and patient tumors, which was responsible for the corresponding transcriptional upregulation of ANGPTL4. These data indicate that the metabolic reprogramming of cancer cells induced by F. nucleatum is essential for its enrichment and persistence in CRC, providing a novel potential target for the clinical intervention of F. nucleatum-related CRC. SignificanceF. nucleatum colonization in colorectal cancer is regulated by ANGPTL4-mediated glycolysis, suggesting targeting this axis as a strategy for combined repression of F. nucleatum and cancer progression.Research.

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Section: F Nucleatum Promotes Angptl4 Expression By Facilitating the H3k27acmentioning

confidence: 97%

ANGPTL4-Mediated Promotion of Glycolysis Facilitates the Colonization ofFusobacterium nucleatumin Colorectal Cancer

Zheng

Zhou

et al. 2021

Cancer Research

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“…Similarly, an increased prevalence of Fusobacterium nucleatum [117], Escherichia coli [118], Streptococcus bovis [119], Streptococcus gallolyticus [119], Bacteroides fragilis [6], species of Dorea [120] and Porphyromonas [120], and a diminished number of Pseudomonas, Prevotella, Acinetobacter, and Catenibacterium [121] are associated with CRC.…”

Section: Git Cancer-associated Microbiotamentioning

confidence: 99%

Bacterial Extracellular Vesicles in Gastrointestinal Tract Cancer: An Unexplored Territory

Amatya

Salmi

Kainulainen

et al. 2021

Cancers

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Bacterial extracellular vesicles are membrane-enclosed, lipid bi-layer nanostructures that carry different classes of biomolecules, such as nucleic acids, lipids, proteins, and diverse types of small molecular metabolites, as their cargo. Almost all of the bacteria in the gut secrete extracellular vesicles to assist them in competition, survival, material exchange, host immune modulation, infection, and invasion. The role of gut microbiota in the development, progression, and pathogenesis of gastrointestinal tract (GIT) cancer has been well documented. However, the possible involvement of bacterial extracellular vesicles (bEVs) in GIT cancer pathophysiology has not been given due attention. Studies have illustrated the ability of bEVs to cross physiological barriers, selectively accumulate near tumor cells, and possibly alter the tumor microenvironment (TME). A systematic search of original published works related to bacterial extracellular vesicles on gastrointestinal cancer was performed for this review. The current systemic review outlines the possible impact of gut microbiota derived bEVs in GIT cancer in light of present-day understanding. The necessity of using advanced sequencing technologies, such as genetic, proteomic, and metabolomic investigation methodologies, to facilitate an understanding of the interrelationship between cancer-associated bacterial vesicles and gastrointestinal cancer is also emphasized. We further discuss the clinical and pharmaceutical potential of bEVs, along with future efforts needed to understand the mechanism of interaction of bEVs in GIT cancer pathogenesis.

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“…P. gingivalis , as the member of Porphyromonas , might be associated with the colorectal cancer. In vitro , P. gingivalis changed the tumor immune environment by selectively expanding myeloid-derived immune cells and induced CRC development by activating hematopoietic nucleotide-binding oligomerization domain receptor and pyrin domain containing 3 (NLRP3) ( 137 ).…”

Section: Effect Of Periodontal Pathogens On the Intestinal Immune Barriermentioning

confidence: 99%

Multifaceted Impacts of Periodontal Pathogens in Disorders of the Intestinal Barrier

et al. 2021

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Periodontal disease, a common inflammatory disease, is considered a hazardous factor that contributes to the development of diseases of the digestive system as well as other systems. The bridge between periodontitis and systemic diseases is believed to be periodontal pathogens. The intestine, as part of the lower gastrointestinal tract, has a close connection with the oral cavity. Within the intestine, the intestinal barrier acts as a multifunctional system including microbial, mucous, physical and immune barrier. The intestinal barrier forms the body’s first line of defense against external pathogens; its breakdown can lead to pathological changes in the gut and other organs or systems. Reports in the literature have described how oral periodontal pathogens and pathobiont-reactive immune cells can transmigrate to the intestinal mucosa, causing the destruction of intestinal barrier homeostasis. Such findings might lead to novel ideas for investigating the relationship between periodontal disease and other systemic diseases. This review summarizes studies on the effects of periodontal pathogens on the intestinal barrier, which might contribute to understanding the link between periodontitis and gastrointestinal diseases.

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Porphyromonas gingivalis Promotes Colorectal Carcinoma by Activating the Hematopoietic NLRP3 Inflammasome

Cited by 112 publications

References 59 publications

ANGPTL4-Mediated Promotion of Glycolysis Facilitates the Colonization ofFusobacterium nucleatumin Colorectal Cancer

ANGPTL4-Mediated Promotion of Glycolysis Facilitates the Colonization ofFusobacterium nucleatumin Colorectal Cancer

Bacterial Extracellular Vesicles in Gastrointestinal Tract Cancer: An Unexplored Territory

Multifaceted Impacts of Periodontal Pathogens in Disorders of the Intestinal Barrier

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