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Open AccessJournal ArticleDOI

Fusobacterium nucleatum Acts as a Pro-carcinogenic Bacterium in Colorectal Cancer: From Association to Causality.

TLDR
In this paper, the authors summarized the biological characteristics of Fusobacterium nucleatum and the epidemiological associations between F. nucleatum, and highlighted the mechanisms by which F.ucleatum participates in CRC progression, metastasis, and chemoresistance by affecting cancer cells or regulating the tumor microenvironment.
Abstract
Colorectal cancer (CRC) is a common cancer worldwide with complex etiology. Fusobacterium nucleatum (F. nucleatum), an oral symbiotic bacterium, has been linked with CRC in the past decade. A series of gut microbiota studies show that CRC patients carry a high abundance of F. nucleatum in the tumor tissue and fecal, and etiological studies have clarified the role of F. nucleatum as a pro-carcinogenic bacterium in various stages of CRC. In this review, we summarize the biological characteristics of F. nucleatum and the epidemiological associations between F. nucleatum and CRC, and then highlight the mechanisms by which F. nucleatum participates in CRC progression, metastasis, and chemoresistance by affecting cancer cells or regulating the tumor microenvironment (TME). We also discuss the research gap in this field and give our perspective for future studies. These findings will pave the way for manipulating gut F. nucleatum to deal with CRC in the future.

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Journal ArticleDOI

Oral microbiota in human systematic diseases

TL;DR: In this article , the authors discussed emerging and exciting evidence of complex and important connections between the oral microbes and multiple human systemic diseases, and the possible contribution of the oral microorganisms to systemic diseases.
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Integrated metagenomic and metabolomic analysis reveals distinct gut-microbiome-derived phenotypes in early-onset colorectal cancer

TL;DR: The predictive model based on metagenomic, metabolomic and KO gene markers achieved a powerful classification performance for distinguishing EO-CRC from controls, suggesting that altered microbiome–metabolome interplay helps explain the pathogenesis of EO.CRC.
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Alterations in the Gut Microbiota and Their Metabolites in Colorectal Cancer: Recent Progress and Future Prospects

TL;DR: Gut microbiota and their metabolites influence the progression and causation of CRC, and the association analysis of metabolomics and gut microbiome will provide novel strategies for the prevention, diagnosis, and therapy of CRC.
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Dysbiosis of skin microbiome and gut microbiome in melanoma progression

TL;DR: In this article , the authors examined associations between dysbiosis in the skin and gut microbiome and the melanoma growth using MeLiM porcine model of melanoma progression and spontaneous regression.
Journal ArticleDOI

Dysbiosis of skin microbiome and gut microbiome in melanoma progression

TL;DR: In this article , the authors examined associations between dysbiosis in the skin and gut microbiome and the melanoma growth using MeLiM porcine model of melanoma progression and spontaneous regression.
References
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Journal ArticleDOI

Fusobacterium nucleatum outer membrane proteins Fap2 and RadD induce cell death in human lymphocytes.

TL;DR: A mechanism employed by the Gram-negative oral pathogen Fusobacterium nucleatum for cell death induction of human lymphocytes via two outer membrane proteins, Fap2 and RadD, which share regions homologous to autotransporter secretion systems (type Va secretion systems).
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Non-coding RNAs in GI cancers: from cancer hallmarks to clinical utility.

TL;DR: This review will present the biology and translational value of three of the most studied categories on non-coding RNAs, the microRNas, the long non-Coding RNas and the circular RNAs.
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HIV persists throughout deep tissues with repopulation from multiple anatomical sources.

TL;DR: HIV reservoirs persist in all deep tissues, and blood is the main source of dispersal, which may explain why eliminating HIV susceptibility in circulating T cells via bone marrow transplants allowed some people with HIV to have therapy free remission, even though deeper tissue reservoirs were not targeted.
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Invasive Fusobacterium nucleatum activates beta-catenin signaling in colorectal cancer via a TLR4/P-PAK1 cascade

TL;DR: The data suggest that invasive Fn activates β-catenin signaling via a TLR4/P-PAK1 /P-β- catenin S675 cascade in CRC, and TLR 4 and PAK1 could be potential pharmaceutical targets for the treatment of Fn-related CRCs.
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