Microbiota dysbiosis: a new piece in the understanding of the carcinogenesis puzzle

García-Castillo, Valeria; Sanhueza, Enrique; McNerney, Eileen M.; Oñate, Sergio A.; García, Antonio Manuel Rodríguez

doi:10.1099/jmm.0.000371

Cited by 102 publications

(80 citation statements)

References 92 publications

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“…Over the last few decades, an increasing body of studies has indicated the assemblage of gut microbiota influences the formation and progression of CRC. [16][17][18][19] However, few studies focus on the difference of gut microbiome in paired tumor and adjacent normal tissues of CRC patients. In this study, we used 16S rRNA sequencing to show the profile of the gut microbiome in Chinese CRC patients.…”

Section: Discussionmentioning

confidence: 99%

<p>Comparison of Gut Microbiome in Human Colorectal Cancer in Paired Tumor and Adjacent Normal Tissues</p>

Sheng

et al. 2020

OTT

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Background: To understand the biological effect of gut microbiome on the progression of colorectal cancer (CRC), we sequenced the V3-V4 region of the 16S rRNA gene to illustrate the overall structure of microbiota in the CRC patients. Methods: In this study, a total of 66 CRC patients were dichotomized into different groups based on the following characteristics: paired tumor and adjacent normal tissues, distal and proximal CRC segments, MMR (-) and MMR (+), different TNM staging and clinic tumor staging. Results: By sequencing and comparing the microbial assemblages, our results indicated that 7 microbe genus (Fusobacterium, Faecalibacterium, Akkermansia, Ruminococcus2, Parabacteroides, Streptococcus, and f_Ruminococcaceae) were significantly different between tumor and adjacent normal tissues; and 5 microbe genus (Bacteroides, Fusobacterium, Faecalibacterium, Parabacteroides, and Ruminococcus2) were significantly different between distal and proximal CRC segments; only 2 microbe genus (f_Enterobacteriaceae and Granulicatella) were significantly different between MMR (-) and MMR (+); but there was no significant microbial difference were detected neither in the TNM staging nor in the clinic tumor staging. Conclusion: All these findings implied a better understanding of the alteration in the gut microbiome, which may offer new insight into diagnosing and therapying for CRC patients.

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Section: Discussionmentioning

confidence: 99%

<p>Comparison of Gut Microbiome in Human Colorectal Cancer in Paired Tumor and Adjacent Normal Tissues</p>

Sheng

et al. 2020

OTT

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“…Such dysbiosis, or disturbance in microbial community membership, structure or function, can consist of a loss of specific beneficial bacteria or a critical loss of diversity among the beneficial bacteria. This produces a state termed a pathobiome, defined as loss of the health‐promoting microbiome with a predominance of disease‐producing pathogens.…”

Section: Microbiome and Tumorigenesismentioning

confidence: 99%

Gut microbiome influences on anastomotic leak and recurrence rates following colorectal cancer surgery

Gaines

Shao

Hyman

et al. 2018

British Journal of Surgery

128

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Background The pathogenesis of colorectal cancer recurrence after a curative resection remains poorly understood. A yet-to-be accounted for variable is the composition and function of the microbiome adjacent to the tumour and its influence on the margins of resection following resection. Methods PubMed was searched for historical as well as current manuscripts dated between 1970 and 2017 using the following keywords: “colorectal cancer recurrence,” “microbiome,” “anastomotic leak,” “anastomotic failure” and “mechanical bowel preparation”. Results There is a substantial and growing body of literature to demonstrate the various mechanisms by which environmental factors act on the microbiome to alter its composition and function with the net result of adversely affecting oncological outcomes following surgery. Some of these environmental factors include diet, antibiotic use, the methods used to prepare the colon for surgery, and the physiological stress of the operation itself. Conclusion Interrogating the intestinal microbiome using next-generation sequencing technology has the potential to influence cancer outcomes following colonic resection.

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“…Lately, the effects of HFD on gut microbiota dysbiosis are widely concerned . Dysbiosis is defined as a disturbance in the microbiome structure, such as loss of beneficial microorganisms, and expansion of pathological microorganisms, promoting the development of CRC . However, the specific mechanisms that how HFD‐induced dysbiosis affects intestinal carcinogenesis remain to be clarified.…”

Section: Introductionmentioning

confidence: 99%

High‐fat diet‐induced dysbiosis mediates MCP‐1/CCR2 axis‐dependent M2 macrophage polarization and promotes intestinal adenoma‐adenocarcinoma sequence

Guo

Song

et al. 2020

J Cellular Molecular Medi

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High‐fat diet (HFD) is a well‐known risk factor for gut microbiota dysbiosis and colorectal cancer (CRC). However, evidence relating HFD, gut microbiota and carcinogenesis is limited. Our study aimed to demonstrate that HFD‐induced gut dysbiosis promoted intestinal adenoma‐adenocarcinoma sequence. In clinical study, we found that HFD increased the incidence of advanced colorectal neoplasia (AN). The expression of monocyte chemoattractant protein 1 (MCP‐1), CC chemokine receptor 2 (CCR2) and CD163 in CRC patients with HFD was significantly higher than that in CRC patients with normal diet. When it comes to the Apcmin/+ mice, HFD consumption could induce gut dysbiosis and promote intestinal carcinogenesis, accompanying with activation of MCP‐1/CCR2 axis that recruited and polarized M2 tumour‐associated macrophages. Interestingly, transfer of faecal microbiota from HFD‐fed mice to another batch of Apcmin/+ mice in the absence of HFD could also enhance carcinogenesis without significant body weight gain and induced MCP‐1/CCR2 axis activation. HFD‐induced dysbiosis could also be transmitted. Meanwhile, antibiotics cocktail treatment was sufficient to inhibit HFD‐induced carcinogenesis, indicating the vital role of dysbiosis in cancer development. Conclusively, these data indicated that HFD‐induced dysbiosis accelerated intestinal adenoma‐adenocarcinoma sequence through activation of MCP‐1/CCR2 axis, which would provide new insight into better understanding of the mechanisms and prevention for HFD‐related CRC.

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Microbiota dysbiosis: a new piece in the understanding of the carcinogenesis puzzle

Cited by 102 publications

References 92 publications

<p>Comparison of Gut Microbiome in Human Colorectal Cancer in Paired Tumor and Adjacent Normal Tissues</p>

<p>Comparison of Gut Microbiome in Human Colorectal Cancer in Paired Tumor and Adjacent Normal Tissues</p>

Gut microbiome influences on anastomotic leak and recurrence rates following colorectal cancer surgery

High‐fat diet‐induced dysbiosis mediates MCP‐1/CCR2 axis‐dependent M2 macrophage polarization and promotes intestinal adenoma‐adenocarcinoma sequence

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