The inflammatory pathogenesis of colorectal cancer

Schmitt, Mark R.; Greten, Florian R.

doi:10.1038/s41577-021-00534-x

Cited by 400 publications

(305 citation statements)

References 171 publications

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“…The development of CRC is often accompanied by inflammation (Schmitt and Greten, 2021). Inflammatory cells and inflammatory cytokines have been considered active tumor factors since they can induce angiogenesis, and stimulate cancer cells proliferation and invasion (West et al, 2015;Galdiero et al, 2018).…”

Section: Fusobacterium Nucleatum Interacts With Cancer Cellsmentioning

confidence: 99%

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

Wang

Liu

et al. 2021

Front. Cell Dev. Biol.

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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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Section: Fusobacterium Nucleatum Interacts With Cancer Cellsmentioning

confidence: 99%

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

Wang

Liu

et al. 2021

Front. Cell Dev. Biol.

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“…Aberrant inflammation is considered as one of the hallmarks of cancer. During the development of CRC, tumor-promoting inflammation induced by gut microbiota usually involves the first two, characterized by the exaggerated production of cytokines by resident innate immune cells and the establishment of an immunosuppressive TME (45)(46)(47). These proinflammatory mediators interact with epithelia to compromise barrier function and further amplify the response by recruiting and activating additional immune cells.…”

Section: Interaction Of Gut Microbiota Metabolites and Crcmentioning

confidence: 99%

Gut Microbiota-Derived Metabolites in Colorectal Cancer: The Bad and the Challenges

Zhang

Qin

et al. 2021

Front. Oncol.

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Accumulating evidence from studies in humans and animal models has elucidated that gut microbiota, acting as a complex ecosystem, contributes critically to colorectal cancer (CRC). The potential mechanisms often reported emphasize the vital role of carcinogenic activities of specific pathogens, but in fact, a series of metabolites produced from exogenous dietary substrates or endogenous host compounds occupy a decisive position similarly. Detrimental gut microbiota-derived metabolites such as trimethylamine-N-oxide, secondary bile acids, hydrogen sulfide and N-nitroso compounds could reconstruct the ecological composition and metabolic activity of intestinal microorganisms and formulate a microenvironment that opens susceptibility to carcinogenic stimuli. They are implicated in the occurrence, progression and metastasis of CRC through different mechanisms, including inducing inflammation and DNA damage, activating tumorigenic signaling pathways and regulating tumor immunity. In this review, we mainly summarized the intimate relationship between detrimental gut microbiota-derived metabolites and CRC, and updated the current knowledge about detrimental metabolites in CRC pathogenesis. Then, multiple interventions targeting these metabolites for CRC management were critically reviewed, including diet modulation, probiotics/prebiotics, fecal microbiota transplantation, as well as more precise measures such as engineered bacteria, phage therapy and chemopreventive drugs. A better understanding of the interplay between detrimental microbial metabolites and CRC would hold great promise against CRC.

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“…Although a large proportion of the immune cells that infiltrate CRCs are of myeloid origin, our understanding of the contribution of the innate immune system on cancer progression is less advanced 53 . Tumor-elicited inflammation is thought to be caused by the breakdown of the epithelial barrier during tumorigenesis that enables microbial products translocate from the intestinal lumen to activate tissue-resident myeloid cells 54,55 . In addition, necrotic cell death as a consequence of hypoxic conditions and lack of sufficient nutrients has been described to induce innate and adaptive immune responses 54 .…”

Section: Discussionmentioning

confidence: 99%

Revisiting colorectal cancer tumorigenesis with spatially-resolved gene expression profiling

Roelands

et al. 2021

Preprint

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Early detection and treatment are paramount to the clinical outcome of patients with colorectal cancer (CRC). Deciphering the dynamic interactions that occur between epithelial cells and stromal cells during tumorigenesis requires in-depth analyses of early-stage CRC lesions in spatial context. Here we employed spatially-resolved gene expression profiling to dissect molecular processes that associate with malignant transformation in CRC. We provide the transcriptional landscapes of colorectal cancer tumorigenesis from healthy mucosa, through different degrees of dysplasia, to cancer. The complementary examination of epithelial and stromal fractions allowed us to define whether specific oncogenic processes involved cancer cells, stromal cells, or the tumor microenvironment as a whole. We identified several genes that were consistently deregulated during CRC onset that could serve as clinical biomarkers for early-stage CRC. Furthermore, we uncovered an essential role for the innate immune system during CRC tumorigenesis.

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The inflammatory pathogenesis of colorectal cancer

Cited by 400 publications

References 171 publications

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

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

Gut Microbiota-Derived Metabolites in Colorectal Cancer: The Bad and the Challenges

Revisiting colorectal cancer tumorigenesis with spatially-resolved gene expression profiling

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