The germ-free mice monocolonization with Bacteroides fragilis improves azoxymethane/dextran sulfate sodium induced colitis-associated colorectal cancer

2019 ◽  
Vol 41 (2) ◽  
pp. 207-213 ◽  
Author(s):  
Yen-Peng Lee ◽  
Chien-Chao Chiu ◽  
Tien-Jen Lin ◽  
Shao-Wen Hung ◽  
Wen-Ching Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Bacteroides Fragilis ◽  
Germ Free

scholarly journals Piperlongumine Alleviates Mouse Colitis and Colitis-Associated Colorectal Cancer

2020 ◽  
Vol 11 ◽  
Author(s):  
Jia-Rong Huang ◽  
Sheng-Te Wang ◽  
Meng-Ning Wei ◽  
Kun Liu ◽  
Jing-Wen Fu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Epithelial Mesenchymal Transition ◽  
Colonic Neoplasms ◽  
Causative Factor ◽  
Therapeutic Effects ◽  
Acute Colitis ◽  
Related Factors ◽  
Mesenchymal Transition

Colorectal cancer is one of the most common and lethal cancers in the world. An important causative factor of colorectal cancer is ulcerative colitis. In this study, we investigated the therapeutic effects of piperlongumine (PL) on the dextran sulfate sodium (DSS)-induced acute colitis and azoxymethane (AOM)/DSS-induced colorectal cancer mouse models. Our results showed that PL could inhibit the inflammation of DSS-induced mouse colitis and reduce the number of large neoplasms (diameter >2 mm) of AOM/DSS-induced mouse colorectal cancer by downregulation of proinflammatory cytokines cyclooxygenase-2 and interleukin-6 and epithelial-mesenchymal transition-related factors, β-catenin, and snail expressions, but fail to improve the colitis symptoms and to decrease the incidence of colonic neoplasms and the number of small neoplasms (diameter <2 mm). These data suggested that PL might be an effective agent in treating colitis and colorectal cancer.

scholarly journals Monocolonization of Germ-Free Mice withBacteroides fragilisProtects against Dextran Sulfate Sodium-Induced Acute Colitis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Chien-Chao Chiu ◽  
Yung-Hao Ching ◽  
Yu-Chih Wang ◽  
Ju-Yun Liu ◽  
Yen-Peng Li ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Interleukin 10 ◽  
Myeloperoxidase Activity ◽  
Acute Colitis ◽  
Germ Free ◽  
Intestinal Immune System ◽  
Anti Inflammatory

Ulcerative colitis is inflammatory conditions of the colon caused by interplay of genetic and environmental factors. Previous studies indicated that the gut microflora may be involved in the colonic inflammation.Bacteroides fragilis(BF) is a Gram-negative anaerobe belonging to the colonic symbiotic. We aimed to investigate the protective role ofBFin a colitis model induced in germ-free (GF) mice by dextran sulfate sodium (DSS). GF C57BL/6JNarl mice were colonized withBFfor 28 days before acute colitis was induced by DSS.BFcolonization significantly increased animal survival by 40%, with less reduction in colon length, and decreased infiltration of inflammatory cells (macrophages and neutrophils) in colon mucosa following challenge with DSS. In addition,BFcould enhance the mRNA expression of anti-inflammatory-related cytokine such as interleukin 10 (IL-10) with polymorphism cytokineIL-17and diminish that of proinflammatory-related tumor necrosis factorαwith inducible nitric oxide synthase in the ulcerated colon. Myeloperoxidase activity was also decreased inBF-DSS mice. Taking these together, theBFcolonization significantly ameliorated DSS-induced colitis by suppressing the activity of inflammatory-related molecules and inducing the production of anti-inflammatory cytokines.BFmay play an important role in maintaining intestinal immune system homeostasis and regulate inflammatory responses.

scholarly journals NUDT7 Loss Promotes KrasG12D CRC Development

Cancers ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 576
Author(s):  
Jinsoo Song ◽  
Sujeong Park ◽  
Jinjoo Oh ◽  
Deokha Kim ◽  
Ji Hyun Ryu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Lipid Metabolism ◽  
Palmitic Acid ◽  
Wnt Signaling ◽  
Ingenuity Pathway Analysis ◽  
Pathway Analysis ◽  
Lipid Accumulation ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Expression Levels

Studies have suggested that dysregulation of peroxisomal lipid metabolism might play an important role in colorectal cancer (CRC) development. Here, we found that KrasG12D-driven CRC tumors demonstrate dysfunctional peroxisomal β-oxidation and identified Nudt7 (peroxisomal coenzyme A diphosphatase NUDT7) as one of responsible peroxisomal genes. In KrasG12D-driven CRC tumors, the expression level of Nudt7 was significantly decreased. Treatment of azoxymethane/dextran sulfate sodium (AOM/DSS) into Nudt7 knockout (Nudt7−/−) mice significantly induced lipid accumulation and the expression levels of CRC-related genes whereas xenografting of Nudt7-overexpressed LS-174T cells into mice significantly reduced lipid accumulation and the expression levels of CRC-related genes. Ingenuity pathway analysis of microarray using the colon of Nudt7−/− and Nudt7+/+ mice treated with AOM/DSS suggested Wnt signaling as one of activated signaling pathways in Nudt7−/− colons. Upregulated levels of β-catenin were observed in the colons of KrasG12D and AOM/DSS-treated Nudt7−/− mice and downstream targets of β-catenin such as Myc, Ccdn1, and Nos2, were also significantly increased in the colon of Nudt7−/− mice. We observed an increased level of palmitic acid in the colon of Nudt7−/− mice and attachment of palmitic acid-conjugated chitosan patch into the colon of mice induced the expression levels of β-catenin and CRC-related genes. Overall, our data reveal a novel role for peroxisomal NUDT7 in KrasG12D-driven CRC development.

scholarly journals 17β-Estradiol strongly inhibits azoxymethane/dextran sulfate sodium-induced colorectal cancer development in Nrf2 knockout male mice

2020 ◽  
Vol 182 ◽  
pp. 114279
Author(s):  
Chin-Hee Song ◽  
Nayoung Kim ◽  
Ryoung Hee Nam ◽  
Soo In Choi ◽  
Joo Hee Son ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Cancer Development ◽  
Male Mice ◽  
Nrf2 Knockout ◽  
17Β Estradiol

scholarly journals Colitis-induced IL11 promotes colon carcinogenesis

2020 ◽  
Author(s):  
Hong Wang ◽  
David H Wang ◽  
Xu Yang ◽  
Yuhai Sun ◽  
Chung S Yang
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Epithelial Cells ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Colon Carcinogenesis ◽  
Human Colorectal Cancer ◽  
Colon Crypt

Abstract Colitis increases the risk of colorectal cancer; however, the mechanism of the association between colitis and cancer remains largely unknown. To identify colitis-associated cancer promoting factors, we investigated gene expression changes caused by dextran sulfate sodium (DSS)-induced colitis in mice. By analyzing gene expression profiles, we found that IL11 was upregulated in DSS-induced colitis tissue and 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP)/DSS-induced colon tumors in mice as well as in human colorectal cancer. By characterizing the activation/phosphorylation of STAT3 (pSTAT3), we found that pSTAT3 was induced transiently in colitis, but maintained at higher levels from hyper-proliferative dysplastic lesions to tumors. Using the IL11 receptor (IL11Rα1) knockout mice, we found that pSTAT3 in the newly regenerated crypt epithelial cells in colitis is abolished in IL11Rα1+/- and -/- mice, suggesting that colitis-induced IL11 activates STAT3 in colon crypt epithelial cells. Moreover, colitis-promoted colon carcinogenesis was significantly reduced in IL11Rα1+/- and -/- mice. To determine the roles of the IL11 in colitis, we found that the inhibition of IL11 signaling by recombinant IL11 antagonist mutein during colitis was sufficient to attenuate colitis-promoted carcinogenesis. Together, our results demonstrated that colitis-induced IL11 plays critical roles in creating cancer promoting microenvironment to facilitate the development of colon cancer from dormant premalignant cells.

scholarly journals PHYTOPREVENTIVE EFFECT OF BUAH MERAH (Pandanus conoideus Lam.) OIL IN COLITIS-ASSOCIATED CARCINOGENESIS

2015 ◽  
Vol 1 (2) ◽  
Author(s):  
Oeij Anindita Adhika
Keyword(s):  
Colorectal Cancer ◽  
Intracellular Signaling ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Molecular Target ◽  
Negative Control ◽  
Histopathological Analysis ◽  
Mice Model ◽  
Chronic Inflammatory Response ◽  
One Way Anova

Colorectal cancer has provided a paradigm for the connection between inflammation and cancer. Modulation of intracellular signaling involved in chronic inflammatory response by anti-inflammatory agents represents an important strategy in molecular target-based chemoprevention. The aim of this research is to study the effect of buah merah oil on  IL-6  serum level and histopathology of colon in colitis-associated cancer (CAC) mice model. BALB/c mice were randomly divided into four groups. The negative control and buah merah control were given aquabidest and buah merah, respectively, without CAC induction. The AOM/DSS control and buah merah treatment were given azoxymethane (AOM) followed by dextran sulfate sodium (DSS) to induce CAC. The AOM/DSS control was given aquabidest while the buah merah treatment was given buah merah. Data were analyzed by One-Way ANOVA continued with Tukey-HSD. The result showed that IL-6 level in mice administrated with buah merah was significantly lower than the AOM/DSS control (p=0.000). Histopathological analysis scores  of colon were analyzed by Kruskal-Wallis continued with Mann-Whitney. The result showed that histopathological analysis score in buah merah treatment was significantly lower than in the AOM/DSS control (p=0.002). Taken together, buah merah oil lowered IL-6 level and histopathological analysis score of colon in CAC mice model. Keywords: CAC, buah merah oil,  IL-6 level, histopathological  analysis scores of  colon

scholarly journals Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

2019 ◽  
Vol 216 (10) ◽  
pp. 2378-2393 ◽  
Author(s):  
Wenhan Zhu ◽  
Naoteru Miyata ◽  
Maria G. Winter ◽  
Alexandre Arenales ◽  
Elizabeth R. Hughes ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gut Microbiota ◽  
Chronic Inflammation ◽  
Mouse Models ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
E Coli ◽  
Gut Colonization ◽  
Gut Microbiota Dysbiosis ◽  
Colitis Model

Chronic inflammation and gut microbiota dysbiosis, in particular the bloom of genotoxin-producing E. coli strains, are risk factors for the development of colorectal cancer. Here, we sought to determine whether precision editing of gut microbiota metabolism and composition could decrease the risk for tumor development in mouse models of colitis-associated colorectal cancer (CAC). Expansion of experimentally introduced E. coli strains in the azoxymethane/dextran sulfate sodium colitis model was driven by molybdoenzyme-dependent metabolic pathways. Oral administration of sodium tungstate inhibited E. coli molybdoenzymes and selectively decreased gut colonization with genotoxin-producing E. coli and other Enterobacteriaceae. Restricting the bloom of Enterobacteriaceae decreased intestinal inflammation and reduced the incidence of colonic tumors in two models of CAC, the azoxymethane/dextran sulfate sodium colitis model and azoxymethane-treated, Il10-deficient mice. We conclude that metabolic targeting of protumoral Enterobacteriaceae during chronic inflammation is a suitable strategy to prevent the development of malignancies arising from gut microbiota dysbiosis.

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