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    Home > Biochemistry News > Microbiology News > Intestinal bacterial disorders contribute to the development of colorectal cancer

    Intestinal bacterial disorders contribute to the development of colorectal cancer

    • Last Update: 2020-12-11
    • Source: Internet
    • Author: User
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    trillions of microorganisms, including bacteria, viruses, fungi and ancient bacteria, live in the human gut, mainly bacteria. So far, more than 1,000 bacteria have been identified in the human gut, and the core bacterium shared by different individuals contains about 160. Various bacterial species coexist in proportion, they are interdependent and competing with each other to maintain the relative balance and stability of the intestinal bacterium.normal, intestinal bacteri groups play an important role in promoting the digestion and absorption of nutrients, maintaining normal physiological function of the intestine and regulating immunity. When the intestinal bacterium is affected by diet, environment, host gene and other factors, it can lead to bacterium imbalance, which can be manifested as changes in bacterium composition, changes in bacterial biological activity, and changes in the position of the human body. These changes can lead to diseases such as inflammatory bowel disease, cardiovascular disease, diabetes and mental illness, as well as cancers such as colorectal cancer.colorectal cancer is one of the leading causes of morbidity and mortality worldwide. The incidence and mortality of colorectal cancer in China are on the rise. According to the 2015 Cancer Statistics of China, the incidence and mortality rate of colorectal cancer in China ranked 5th among all malignant tumors. In economically developed cities, the incidence of colorectal cancer appears to be higher. Colorectal cancer is a multi-factor malignant disease, and numerous studies have shown that the causes of colorectal cancer include genetic background and environmental risk factors such as diabetes, gallbladder excision, obesity, high-fat diets, processed foods, red meat, and so on. Over the past decade or so, more and more studies have found the important role of gut microbiomes in the development and development of colorectal cancer, and the causal relationship between the presence of certain microorganisms and the occurrence of colorectal cancer has been verified.a major feature of the microbial intestinal microbiome disorder associated with colorectal cancer is a change in the composition of the gut bacteria, which is characterized by a decrease in beneficial bacteria and an increase in pathogenic bacteria. Intestinal bacteribus disorders can lead to changes in host physiological function, leading to the occurrence of a variety of diseases. A growing body of research has shown a link between intestinal bacteria disorders and colorectal cancer, and significant bacterial disorders usually occur in colorectal cancer tissue and adjacent mucous membranes. Now, some of the key bacteria associated with colorectal cancer are also being revealed.Bacillus ais a Gloran-negative anaerobic bacteria. Ocythrobacteria is a member of the oral flora, commonly found in periodontology, rarely found in the intestines of normal people. Levels of OCS in colon adenoma and colorectal cancer increased, while high levels of OCS were associated with lymph node metastasis in colorectal cancer.can promote colorectal cancer by reducing the number of CD4-plus T cells and reducing THEX protein expression and inhibiting the anti-tumor immune response.Bacillus nucleus secretes Fad A adhesive, which adheres to an extracellular region of a trans-membrane protein called E-cadherin that adheres to the epithelial cells of the intestine, stimulating inflammatory signaling path paths, leading to inflammatory responses and cancerous activation, and stimulating the growth of colorectal cancer cells.The Fap2 protein onBacillus nucleus can bind to T-cells and the inhibitory subject TIGIT on natural killer cells, inhibit tumor cell killing mediated by T-cell activation and natural killer cells, and promote tumor cell proliferation, leading to colorectal cancer.of enterotoxin-producingis a Terrain-negative anaerobic bacteria. The toxins it produces are involved in inflammatory-associated diarrhea or inflammation-induced tumor formation.Fragile mycobacterial toxin is a zinc-dependent metal protease toxin that binds to a subject on the colon epithelial cells, thereby increasing mucosal permeability and cytokine secretion, and then participates in various signal transductivity of colon epithelial cells to promote colorectal cancer through inflammation-adenoma-adenocarcinoma.addition, fragile mycobactertoxins can promote bone marrow cells to bone marrow-sourced inhibit cell differentiation, which in turn induces the occurrence of colorectal cancer through pathogenic inflammatory pathogenesis.E. coliis a human intestinal symbic bacteria, belonging to Glorene negative anaerobic bacteria. Studies have shown that E. coli can be implanted on the colon mucosa, it can increase mucosal permeability in a variety of ways, thereby inducing the occurrence of colorectal cancer. E. coli can be divided into at least 5 subsypes: A, B1, B2, D and E. According to a study involving animal tumor models associated with xenotype transplantation and inflammation, E. coli's B2 subtype has a conservative gene island called polykonygenase (pks), which produces an E. coli gene toxin called colibactin. This genetic toxin can penetrate the colon cell membrane and migrate to the nucleation of the cell, where it can cause DNA double-stranded fractures, cell cycle stagnation and incomplete DNA repair, causing chromosomal distortion and ultimately cancer. salmonella is a group of Glage-negative anaerobic bacteria, commonly found in humans and animals. Common sources of salmonella infection include contaminated foods such as meat, eggs and agricultural products. After salmonella infection, some chronic complications may occur, including reactive arthritis, irritable bowel syndrome, inflammatory bowel disease, or cancer. salmonella secretes the effect protein AvrA, which promotes acetylation and ubimination of the target protein. AvrA inhibits β-catenin, maintains the stability of β-catenin, and promotes the proliferation of intestinal cortectal cells, thereby promoting tumor development. In addition, AvrA can increase tumor diversity and promote tumor processes. other bacteria, Desulfurization Desulfurization Vibrians and Enterococcus faecalis, are Glolfoccus-negative and Glorene-positive anaerobic, respectively. These bacteria may be associated with colorectal cancer because their metabolites hydrogen sulfide and superoxide free-form anions have potential harm to the rectal mucosa. addition, studies have reported the presence of Parvimonas micra anaerobicemia in colon cancer patients. Other studies have observed the abundance of microcytobacteria and Solobacterium Moorei in early-stage patients with colorectal cancer. These studies show that P. micra and S. Moorei may be associated with colorectal cancer. bacterial metabolites associated with colorectal cancer seed fatty acids and gut bacteria ferment dietary fiber to produce short-chain fatty acids, including acetic acid, propic acid, butyric acid, and pyric acid. Short-chain fatty acids can support the health of the intestinal bacterium and increase its diversity. In addition, short-chain fatty acids play an active role in maintaining the function of the intestinal barrier by promoting mucus production and the expression of tightly connected proteins. Short-chain fatty acids also help maintain a healthy immune system. Because of these functions, short-chain fatty acids have a preventive effect on the occurrence of colorectal cancer. The lack of short-chain fatty acids may increase the risk of colorectal cancer. short-chain fatty acids can inhibit colitis and associated cancers by binding to their subject Gpr109a. Butyric acid, as one of the most important members of the family of short-chain fatty acids, exerts anti-inflammatory and anti-tumor properties through cell metabolism, bacterial stabilization, immunomodulation and gene-on-the-surface genetic regulation. Studies have shown that butyric acid can regulate gene expression by inhibiting histoprotein deacetylation, promoting the apoptosis of colorectal cancer cells. other metabolites other metabolites of gut bacteria, including secondary bile acid (deoxycholic acid and stabolic acid), have also been shown to be associated with colorectal cancer. Anaerobic gut bacteria dehydrate the primary bile acid remaining in the intestines into deoxycholic acid and staic acid, which can cause DNA damage by producing freelance fundamentals, increasing the risk of colorectal cancer. , for example, a high-fat diet can lead to an increase in the synthesis of primary bile acid in the liver, which in turn increases the accumulation of bile acid in the intestines. Primary bile acid is converted into secondary bile acid under the metabolism of the intestinal bacterium. Secondary bile acid, especially deoxycholic acid, has genotoxicity, which can cause DNA damage to the epithelial cells of the intestinal mucosa and promote the development of intestinal tumors. In addition, other harmful compounds produced by gut bacteria may also play a role in colorectal cancer and inflammatory bowel disease, such as ammonia, phenol, methylphenol, certain amines and hydrogen sulfide may be involved in the development or exacerbation of cancer through chronic inflammation and DNA damage. possible mechanisms inflammatory responses that drive colorectal cancer in the intestinal bacteriological disorder form a delicate balance between intestinal symblosis and immune cells in the normal intestine. In the case of intestinal bacteria disorders, the activation of inflammatory path roads mediated by inflammatory micro-environments is the driving force behind the development of colorectal cancer. Immune cells in the micro-environment and the cytokines and growth factors they produce activate the associated signaling path path, affecting the self-renewal of the epithelocytos of the colon mucosa, and they also affect colon tissue repair and immune stability. In addition, they can affect the silk division and survival of colon cells. -producing enterotoxin fragile anthocyst can improve the level of intestinal epidermis cell degeneration factors L20 and prostetin E2, prosthetic e2 involved in the proliferation and active of Th17 cells, enhance Th17 cell secretion of IL-17 and related factors, leading to inflammation-related colorectal cancer. intestinal bacterial disorders induce the production of tumor-related genetic toxins and metabolites, which in turn can lead to immune system dysfunction, promote and maintain inflammatory bowel disease, leading to colorectal cancer. immune close contact between the intestinal bacteria and the mucosal immune system also stimulates the immune response of tumors through endogenous bacteria. Th17 immunity is usually carcinogenic and is associated with a poor prognostofectant of colorectal cancer, and its activation can be driven by gut microbes and their products. For example, the Fap2 protein on Bacillus difficile can bind to TIGIT, an inhibitory subject on T-cells and natural killer cells, resulting in the loss of functionality of tumor-killing lymphocytes. 。 DNA damage accumulation of DNA damage can lead to the destruction of host genome stability, which in turn promotes precancer lesions and cancer cells to maintain or accelerate mutations. Gut microbes are a potential source of DNA mutations. In vitro and in vivo studies, for example, have shown that some enterococcals can produce reactive oxygen substances such as hydroxyl free radicals, which cause DNA fractures, point mutations, and protein-DNA interlinking, reducing the stability of genes associated with colorectal cancer. Various animal models of colorectal cancer have also confirmed that enterotoxin-producing fragile pythons induce the expression of colon endodermic amine oxidase, which can cause DNA damage. In addition, pks-positive E. coli promotes DNA double-stranded fracture, cell cycle blocking, and non-regal cell division in the body. intestinal bacterioscopic disorders can directly or indirectly cause DNA damage, affect genomic stability, and make intestinal bacteriocytosis a potential risk factor and therapeutic target for colorectal cancer. cell proliferation in normal tissues, growth and death-induced signals are strictly regulated to maintain cell structure and function. Once cell proliferation and apoptosis signals are disturbed, leading to the continued proliferation of cells, malignant tumors eventually develop. infection can cause excessive proliferation and differentiation of intestinal stem cells in mice by activating certain signaling path path paths. Fragile mycobacterial toxins produced by the fragile Bacillus can promote colonal cortation. Bacillus difficile can also be combined with the cross-membrane protein E-cadherin on the epithelial of the intestine through FadA, which activates downstream pathstream pathstreams and promotes epithelial cell proliferation. As a result, abnormal intestinal bacteri groups activate abnormal cortation cell proliferation and promote early tumor occurrence. Summary Intestinal bactericus are involved in the body's nutritional, metabolic and immune functions, intestinal microbiotic disorders can lead to changes in cytosyte composition and activity, and specific microbiotics and their metabolites may induce the occurrence and process of colorectal cancer in different ways, such as promoting inflammatory responses, inducing DNA damage, or promoting cell proliferation. There are significant differences in fecal virloids in colorectal cancer patients and healthy individuals, so intestinal virlotas are also known as an important marker of the risk of colorectal cancer and can be used for early screening for colorectal cancer and precancerog lesions. Specific gut bacteria and their metabolites will provide new strategies for the prediction, prevention and treatment of colorectal cancer. references:
    Fan, X., et al. (2020). "Gut Microbiota Dysbiosis Drives the Development of Colorectal Cancer." Digestion: 1-8.
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