Smoking is a major risk factor for colorectal cancer (CRC)

Yu Jun's team from The Chinese University of Hong Kong published a paper in Gut (IF=32) titled "Cigarette smoke promotes colorectal cancer through modulation of gut microbiota and related metabolites" on April 6, 2022, in which C57BL/6 mice treated with azomethane were exposed to cigarette smoke or clean air for 2 hours per day for 28 weeks. The study discovered a significant increase in tumor incidence and cell proliferation in cigarette-smoking mice compared to non-smoking control mice.

Dysbiosis of the intestinal microflora was observed in mice exposed to smoke, with significant differences in the abundance of bacterial species, including enrichment of Eggerthella lenta and depletion of Parabacteroides distasonis and Lactobacillus spp. Metabolomic analysis revealed increased bile acid metabolites, particularly taurodeoxycholic acid (TDCA), in the colon of mice exposed to smoke. This study found that E. lenta had the most positive correlation with TDCA in smoke-exposed mice.

Furthermore, smoke-exposed mice had increased oncogenic MAPK/ERK signaling (a downstream target of TDCA) as well as impaired intestinal barrier function. Furthermore, colon cell proliferation was increased in germ-free mice transplanted with smoke-exposed mice feces (GF-AOMS). Similarly, GF-AOMS showed increased abundance of intestinal E. coli and TDCA, activation of the MAPK/ERK pathway, and impaired intestinal barrier in the colonic epithelium.

In conclusion, this study discovered that cigarette smoke-induced gut flora dysbiosis promotes colorectal cancer. Smoke-induced intestinal dysbiosis alters intestinal metabolites and impairs intestinal barrier function, which may activate oncogenic MAPK/ERK signaling in the colonic epithelium.

CRC is one of the most common cancers worldwide. Although there are many strategies for early CRC screening and prevention, the burden is expected to increase further. Evidence supports an association between lifestyle and CRC, such as diet, smoking, obesity, and exercise.

Smoking increases the risk of lung cancer, and about 80% of primary lung cancers can be attributed to smoking. Tobacco use also raises the risk of cancer in organs that are not directly exposed to cigarette smoke, such as the colon, rectum, pancreas, and kidneys. Smoking has been shown in studies to be significantly associated with CRC incidence and mortality in humans, and it has also been shown in animal models to increase the risk of CRC development. The mechanisms by which smoking promotes the development and progression of colorectal cancer, on the other hand, are unknown.

Increased bacterial diversity was observed in humans after smoking cessation. The study also suggests that alterations in microbiome and mucin structure are associated with smoking. In addition, gut microbes from CRC patients can promote colonic tumorigenesis in recipient mice. However, whether alterations in the gut microbiota represent a link between smoking and colorectal cancer remains elusive.

In conclusion, this study found that cigarette smoke-induced gut flora dysbiosis has a pro-tumor effect in colorectal cancer. Smoke-induced intestinal dysbiosis alters intestinal metabolites and impairs intestinal barrier function, which may activate oncogenic MAPK/ERK signaling in the colonic epithelium.

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