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When it comes to cancer, everyone is afraid.
In our daily life, many bad habits can lead to the occurrence of cancer, such as smoking.
Does smoking really cause cancer? How much do you know about smoking causing cancer?
In our daily life, many bad habits can lead to the occurrence of cancer, such as smoking.
Does smoking really cause cancer? How much do you know about smoking causing cancer?
Cigarette smoke contains a lot of harmful substances, which can cause a lot of harm to the human body after inhalation.
For example, smoking increases the risk of lung cancer.
About 80% of primary lung cancers can be attributed to smoking.
In addition, smoking It also increases the risk of cancer in other organs that are not directly exposed to cigarette smoke
.
Smoking has been shown to be significantly associated with human colorectal cancer (CRC) morbidity and mortality, and gut microbes from CRC patients can promote colorectal tumorigenesis in recipient mice
.
However, the mechanism by which smoking promotes the development and progression of colorectal cancer is unclear, and whether alterations in the gut microbiota represent the link between smoking and CRC remains unclear
.
Baiqu Biometabolomics assisted the team of Prof.
Jun Yu of the Chinese University of Hong Kong to publish a paper entitled "Cigarettesmoke promotes colorectal cancer through modulation of gut microbiota and related metabolites" on Gut (IF=31.
793).
Provides LC-MS non-target metabolome + bile acid target detection and analysis services
.
For example, smoking increases the risk of lung cancer.
About 80% of primary lung cancers can be attributed to smoking.
In addition, smoking It also increases the risk of cancer in other organs that are not directly exposed to cigarette smoke
.
Smoking has been shown to be significantly associated with human colorectal cancer (CRC) morbidity and mortality, and gut microbes from CRC patients can promote colorectal tumorigenesis in recipient mice
.
However, the mechanism by which smoking promotes the development and progression of colorectal cancer is unclear, and whether alterations in the gut microbiota represent the link between smoking and CRC remains unclear
.
Baiqu Biometabolomics assisted the team of Prof.
Jun Yu of the Chinese University of Hong Kong to publish a paper entitled "Cigarettesmoke promotes colorectal cancer through modulation of gut microbiota and related metabolites" on Gut (IF=31.
793).
Provides LC-MS non-target metabolome + bile acid target detection and analysis services
.
Research result
1.
Cigarette smoke promotes the development of colorectal cancer in mice
Cigarette smoke promotes the development of colorectal cancer in mice
To investigate the effect of smoking on colorectal tumor formation, C57BL/6 mice were exposed to cigarette smoke for 28 days (2 h/d, Figure 1A) using azomethane oxide (AOM)
.
Compared with smoke-free control mice, mice exposed to cigarette smoke had significantly increased number and size of colorectal tumors (Fig.
1B), increased incidence (Fig.
1D), and increased proliferation of colorectal epithelial cells (Fig.
1E- F)
.
.
Compared with smoke-free control mice, mice exposed to cigarette smoke had significantly increased number and size of colorectal tumors (Fig.
1B), increased incidence (Fig.
1D), and increased proliferation of colorectal epithelial cells (Fig.
1E- F)
.
Figure 1.
Cigarette smoke increases the carcinogenicity of colorectal cancer in mice
Cigarette smoke increases the carcinogenicity of colorectal cancer in mice
2.
Cigarette smoke alters gut microbiota composition and microbial interactions in mice
Cigarette smoke alters gut microbiota composition and microbial interactions in mice
After using 16S sequencing to rule out the effect of cage effects on the gut microbiota of the mice in this experiment, metagenomic sequencing identified potential changes in the gut microbiota induced by cigarette smoke exposure
.
Mice exposed to cigarette smoke had lower alpha diversity compared to smokeless control mice (Fig.
2A)
.
β-diversity results showed that the gut microbiota clustering was significantly different between smoke-exposed mice and control mice (Fig.
2B)
.
20 kinds of intestinal bacteria changed significantly, among which E.
lenta was significantly enriched and intestinal beneficial bacteria decreased (Fig.
2C-D)
.
The interaction between microorganisms may affect the development of disease.
The ecological network diagram of the interaction between bacteria with different abundances in different treatment groups was analyzed, and it was found that there was an antagonism between the enriched E.
lenta and the decreased intestinal beneficial bacteria relationship (Figure 2E)
.
.
Mice exposed to cigarette smoke had lower alpha diversity compared to smokeless control mice (Fig.
2A)
.
β-diversity results showed that the gut microbiota clustering was significantly different between smoke-exposed mice and control mice (Fig.
2B)
.
20 kinds of intestinal bacteria changed significantly, among which E.
lenta was significantly enriched and intestinal beneficial bacteria decreased (Fig.
2C-D)
.
The interaction between microorganisms may affect the development of disease.
The ecological network diagram of the interaction between bacteria with different abundances in different treatment groups was analyzed, and it was found that there was an antagonism between the enriched E.
lenta and the decreased intestinal beneficial bacteria relationship (Figure 2E)
.
Figure 2.
Modulation of the gut microbiota in mice by cigarette smoke
Modulation of the gut microbiota in mice by cigarette smoke
3.
Cigarette smoke alters gut microbe-related metabolites in feces
Cigarette smoke alters gut microbe-related metabolites in feces
Analysis of mouse fecal metabolomics, off-target metabolomics results showed that the metabolic profile of cigarette smoke-exposed mice was significantly different from that of smoke-free mice (Figure 3A-B)
.
The main enrichment pathway of differential metabolites was the bile acid biosynthesis pathway, and the bile acid target validation results showed that the cancer-promoting taurodeoxycholic acid (TDCA) was significantly increased in cigarette smoke-exposed mice (Fig.
3C–D)
.
Correlation analysis of microorganisms and metabolites showed that the abundance of E.
lenta was positively correlated with TDCA concentrations in feces (Fig.
3E–F)
.
These results suggest that dysbiosis of gut microbes and altered metabolites may work together to develop colorectal cancer
.
.
The main enrichment pathway of differential metabolites was the bile acid biosynthesis pathway, and the bile acid target validation results showed that the cancer-promoting taurodeoxycholic acid (TDCA) was significantly increased in cigarette smoke-exposed mice (Fig.
3C–D)
.
Correlation analysis of microorganisms and metabolites showed that the abundance of E.
lenta was positively correlated with TDCA concentrations in feces (Fig.
3E–F)
.
These results suggest that dysbiosis of gut microbes and altered metabolites may work together to develop colorectal cancer
.
Figure 3.
Cigarette smoke alters gut microbe-associated metabolites in feces
Cigarette smoke alters gut microbe-associated metabolites in feces
4.
Cigarette smoke impairs intestinal barrier function and enhances the expression of oncogenic signaling and pro-inflammatory signaling genes in the colorectal epithelium
Cigarette smoke impairs intestinal barrier function and enhances the expression of oncogenic signaling and pro-inflammatory signaling genes in the colorectal epithelium
By measuring the expression levels of colorectal claudin and serum lipopolysaccharide (LPS) levels, it was found that exposure to cigarette smoke resulted in a significant decrease in the levels of claudin-3 and ZO-1, and a significant increase in serum LPS, which reflects cigarette smoke.
Smoke leads to impaired intestinal barrier function (Figure 4)
.
Smoke leads to impaired intestinal barrier function (Figure 4)
.
Figure 4.
Cigarette smoke impairs gut barrier function
Cigarette smoke impairs gut barrier function
Further molecular level studies showed that cigarette smoke exposure induced increased phosphorylation of key mediator proteins ERK1/2 in the MAPK/ERK pathway, activated the MAPK/ERK signaling pathway, and promoted colorectal tumorigenesis (Fig.
5A-C)
.
In addition, cigarette smoke exposure also induces changes in signaling pathways such as interleukin 17 (IL-17) and tumor necrosis factor (TNF), resulting in an increase in the expression of pro-inflammatory factors and a decrease in the expression of anti-inflammatory factors, which promotes the development of colorectal cancer.
inflammation (Figure 5D-F)
.
5A-C)
.
In addition, cigarette smoke exposure also induces changes in signaling pathways such as interleukin 17 (IL-17) and tumor necrosis factor (TNF), resulting in an increase in the expression of pro-inflammatory factors and a decrease in the expression of anti-inflammatory factors, which promotes the development of colorectal cancer.
inflammation (Figure 5D-F)
.
Figure 5.
Cigarette smoke enhances oncogenic MAPK/ERK and pro-inflammatory pathways in colorectal epithelium
Cigarette smoke enhances oncogenic MAPK/ERK and pro-inflammatory pathways in colorectal epithelium
5.
Fecal microbial transplantation in germ-free mice reproduces gut microbiota changes in a conventional mouse model
Fecal microbial transplantation in germ-free mice reproduces gut microbiota changes in a conventional mouse model
To confirm the direct role of cigarette smoke altering gut microbiota in colorectal cancer formation, we performed fecal microbiota transplantation in germ-free mice (Fig.
6A)
.
Germ-free mouse metagenomic sequencing results were similar to conventional mouse sequencing results in germ-free mice fed faeces from cigarette smoke-exposed mice (GF-AOM) compared to germ-free mice fed faeces from smoke-free mice (GF-AOM).
The α-diversity of GF-AOMS) was significantly reduced, and the β-diversity analysis showed a significant separation of gut microbiota between the two groups of germ-free mice after fecal transplantation, E.
lenta was significantly enriched, and intestinal beneficial bacteria were reduced ( Figure 6B-E)
.
The content of TDCA was significantly increased in the feces of GF-AOMS mice (Fig.
6H)
.
In addition, analysis of two mouse models showed that the ecological network modules were more conserved in germ-free mice after fecal transplantation compared with donor mice (Fig.
6G)
.
6A)
.
Germ-free mouse metagenomic sequencing results were similar to conventional mouse sequencing results in germ-free mice fed faeces from cigarette smoke-exposed mice (GF-AOM) compared to germ-free mice fed faeces from smoke-free mice (GF-AOM).
The α-diversity of GF-AOMS) was significantly reduced, and the β-diversity analysis showed a significant separation of gut microbiota between the two groups of germ-free mice after fecal transplantation, E.
lenta was significantly enriched, and intestinal beneficial bacteria were reduced ( Figure 6B-E)
.
The content of TDCA was significantly increased in the feces of GF-AOMS mice (Fig.
6H)
.
In addition, analysis of two mouse models showed that the ecological network modules were more conserved in germ-free mice after fecal transplantation compared with donor mice (Fig.
6G)
.
Figure 6.
Germ-free mouse gut microbiota after transplantation of fecal microbiota from common mice exposed to smoke
Germ-free mouse gut microbiota after transplantation of fecal microbiota from common mice exposed to smoke
6.
Cigarette smoke exposure alters gut microbiota in germ-free mice
Cigarette smoke exposure alters gut microbiota in germ-free mice
Compared with the GF-AOM group, the proliferation of colorectal epithelial cells in the mice in the GF-AOMS group was significantly increased (Fig.
7A-B)
.
The microbiota altered by cigarette smoke also affected the intestinal barrier function of germ-free mice, with decreased expression of tight junction proteins, increased LPS levels, and impaired intestinal barrier function in mice in the GF-AOMS group (Fig.
7C-E)
.
This result is consistent with results from conventional mouse models, suggesting that cigarette smoke-induced changes in microbiota and metabolites impair gut barrier function, which may further promote tumorigenesis
.
Further molecular-level studies found results consistent with conventional mouse models: cigarette smoke-altered microbiota induced TNF and IL-17 signaling and oncogenic MAPK/ERK signaling (Fig.
7F–K)
.
These results suggest that alterations in the gut microbiota induced by cigarette smoke contribute to the development of colorectal cancer
.
7A-B)
.
The microbiota altered by cigarette smoke also affected the intestinal barrier function of germ-free mice, with decreased expression of tight junction proteins, increased LPS levels, and impaired intestinal barrier function in mice in the GF-AOMS group (Fig.
7C-E)
.
This result is consistent with results from conventional mouse models, suggesting that cigarette smoke-induced changes in microbiota and metabolites impair gut barrier function, which may further promote tumorigenesis
.
Further molecular-level studies found results consistent with conventional mouse models: cigarette smoke-altered microbiota induced TNF and IL-17 signaling and oncogenic MAPK/ERK signaling (Fig.
7F–K)
.
These results suggest that alterations in the gut microbiota induced by cigarette smoke contribute to the development of colorectal cancer
.
in conclusion
This study is the first to demonstrate that cigarette smoke promotes colorectal tumorigenesis by inducing gut microbiota dysbiosis
.
Cigarette smoke-induced gut microbiota dysbiosis alters gut metabolites and damages gut barrier function, activates oncogenic MAPK/ERK signaling and pro-inflammatory IL-17 and TNF signaling pathways in colorectal epithelium, and promotes colorectal cancer development (Fig.
8)
.
.
Cigarette smoke-induced gut microbiota dysbiosis alters gut metabolites and damages gut barrier function, activates oncogenic MAPK/ERK signaling and pro-inflammatory IL-17 and TNF signaling pathways in colorectal epithelium, and promotes colorectal cancer development (Fig.
8)
.
Baiqu Biotech provided LC-MS non-target metabolome + bile acid target detection and analysis services for this study, with accurate qualitative and quantitative, built a standard curve of the substance, and provided the absolute content of the substance; the technology is mature and stable, with high resolution and good selectivity; The team is experienced and has a professional R&D and data analysis team
.
Teachers who are interested in using LC-MS non-target metabolome + bile acid target detection for sample detection and analysis are welcome to contact the service hotline: 400-664-9912
.
.
Teachers who are interested in using LC-MS non-target metabolome + bile acid target detection for sample detection and analysis are welcome to contact the service hotline: 400-664-9912
.
