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Evodiamine inhibits high-fat diet-induced colitis-associated cancer in mice through regulating the gut microbiota

Journal of Integrative Medicine 2021年第1期19卷 56-65页

作者： Li-qing Zhu Li Zhang Jia Zhang Guo-lin Chang Gang Liu Dan-dan Yu Xiao-min Yu Mi-sheng Zhao Bin Ye Department of Pathogenic Biology Chongqing Medical UniversityChongqing 400016China Research Center for Molecular Medicine and TumorChongqing Medical UniversityChongqing 400016China Department of Clinical LaboratoryThe First Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325023Zhejiang ProvinceChina Department of PathophysiologyChongqing Medical UniversityChongqing 400016China Department of Clinical LaboratoryWenzhou People’s HospitalWenzhou 325023Zhejiang ProvinceChina Department of EmergencyUniversity-Town Hospital of Chongqing Medical UniversityChongqing 401331China

Objective:High-fat diet is one of the main risk factors that disrupt the balance of gut microbiota,which eventually will induce colorectal cancer(CRC).Evodiamine(EVO)is a wildly used multifunctional traditional Chinese medicine *** this study,we investigated the role of gut microbiota in high-fat dietpropelled CRC and the potential of EVO for CRC ***:Gut microbiota,serum D-lactic acid and endotoxin from 38 patients with colon cancer and 18 healthy subjects were detected by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay(ELISA).In addition,body mass index,phospho-signal transducer and activator of transcription 3(p-STAT3)expression in cancer tissues and paracancerous tissues were detected by immunohistochemistry.A mouse intestinal inflammatory tumor model was established by azomethane/sodium dextran sulfate,followed by treatment with EVO and 5-aminosalicylic acid(ASA).Gut microbiota and inflammatory factors were detected by quantitative polymerase chain reaction,while serum D-lactic acid and endotoxin were detected by ***,cell proliferation,cell apoptosis,and interleukin(IL)-6/STAT3/P65 pathway were evaluated by 5-ethynyl-20-deoxyuridine,terminal-deoxynucleotidyl transferase-mediated nick-end labeling,and Western blot ***:In patients with colon cancer,the numbers of Enterococcus faecalis and Escherichia coli were increased,while those of Bifidobacterium,Campylobacter and Lactobacillus were *** endotoxin and D-lactic acid levels and p-STAT3 levels were significantly *** the mouse model,both EVO and ASA inhibited tumor formation,decreased the proliferation of tumor cells,and induced apoptosis of tumor *** with the control group,the numbers of *** and *** were decreased,while Bifidobacterium,Campylobacter and Lactobacillus numbers were *** the EVO group,serum endotoxin and D-lactic acid levels and inflammatory factors were signifi

关键词： Evodiamine Gut microbiota colitis-associated cancer Signal transducer and activator of transcription 3

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Mitochondrial transcription factor A plays opposite roles in the initiation and progression of colitis-associated cancer

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cancer Communications 2021年第8期41卷 695-714页

作者： Shirong Yang Xianli He Jing Zhao Dalin Wang Shanshan Guo Tian Gao Gang Wang Chao Jin Zeyu Yan Nan Wang Yongxing Wang Yilin Zhao Jinliang Xing Qichao Huang State Key Laboratory of cancer Biology and Department of Physiology and Pathophysiology Fourth Military Medical UniversityXi’anShaanxi 710032P.R.China Department of General Surgery Tangdu HospitalFourth Military Medical UniversityXi’anShaanxi 710032P.R.China Department of Hepatobiliary Surgery Xijing HospitalFourth Military Medical UniversityXi’anShaanxi 710032P.R.China Department of Respiratory Medicine Xijing HospitalFourth Military Medical UniversityXi’anShaanxi 710032P.R.China

Background:Mitochondria are key regulators in cell proliferation and *** in mitochondrial function are closely associated with inflammation and *** study aimed to investigate whether mitochondrial transcription factor A(TFAM),a key regulator of mitochondrial DNA transcription and replication,is involved in the initiation and progression of colitis-associated cancer(CAC).Methods:TFAM expression was examined in tissue samples of inflammatory bowel diseases(IBD)and CAC by *** epithelial cell(IEC)-specific TFAM-knockout mice(TFAM^(△IEC))and colorectal cancer(CRC)cells with TFAM knockdown or overexpression were used to evaluate the role of TFAMin colitis and the initiation and progression *** underlying mechanisms of TFAMwere also explored by analyzingmitochondrial respiration function and ***:The expression of TFAM was downregulated in active IBD and negatively associated with the disease *** downregulation of TFAM in IECs was induced by interleukin-6 in a signal transducer and activator of transcription 3(STAT3)/miR-23b-dependent *** addition,TFAM knockout impaired IECturnover to promote dextran sulfate sodium(DSS)-induced colitis *** note,TFAMknockout increased the susceptibility of mice to azoxymethane/DSSinduced CAC and TFAM overexpression protected mice from intestinal inflammation and colitis-associated *** contrast,TFAM expression was upregulated in CAC tissues and contributed to cell ***,it was demonstrated that β-catenin induced the upregulation of TFAM through c-Myc in CRC ***,TFAMpromoted the proliferation of both IECs and CRC cells by increasing mitochondrial biogenesis and ***:TFAM plays a dual role in the initiation and progression of CAC,providing a novel understanding of CAC pathogenesis.

关键词： colitis colitis-associated cancer colorectal cancer energy metabolism inflammatory bowel diseases intestinal homeostasis mitochondrial transcription factor A(TFAM)

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Lactobacillus bulgaricus inhibits colitis-associated cancer via a negative regulation of intestinal inflammation in azoxymethane/dextran sodium sulfate model

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World Journal of Gastroenterology 2020年第43期26卷 6782-6794页

作者： Denise Sayuri Calheiros Silveira Luciana Chain Veronez Luis Carlos Lopes-Junior Elen Anatriello Mariangela Ottoboni Brunaldi Gabriela Pereira-da-Silva Department of Biochemistry and Immunology University of São Paulo at Ribeirão Preto Medical SchoolRibeirão Preto 14049-900SPBrazil Health Sciences Center Federal University of Espírito Santo-UFESVitória 29043-900ESBrazil Institute of Science and Technology Federal University of São PauloUNIFESPSão Josédos Campos 12231-280SPBrazil Department of Pathology and Forensic Medicine University of São PauloRibeirao Preto 14040-902SPBrazil Department of Maternal-Infant Nursing and Public Health University of São Paulo at Ribeirão Preto College of NursingRibeirão Preto 14040-902SPBrazil

BACKGROUND colitis-associated cancer(CAC)accounts for 2%-3%of colorectal cancer(CRC)cases preceded by inflammatory bowel diseases(IBD)such as Crohn's disease and ulcerative *** microbiota has been reported to play a central role in the pathogenesis of IBD and ***,numerous prebiotics and probiotics have being investigated as antitumor agents due to their capacity to modulate inflammatory *** studies have indicated that lactic acid bacteria could be successfully used in managing sporadic CRC,however little is known about their role in *** To investigate the effect of the probiotic Lactobacillus bulgaricus(***)during the development of an experimental model of colitis associated colon cancer(CAC).METHODS C57BL/6 mice received an intraperitoneal injection of azoxymethane(10 mg/kg),followed by three cycles of sodium dextran sulphate diluted in water(5%w/v).Probiotic group received daily *** inflammation was determined by scoring clinical *** levels were determined from colon and/or tumor samples by ELISA BD OptEIATM *** level of significance was set at P<*** were generated and statistical analysis performed using the software GraphPad Prism *** *** treatment inhibited of total tumor volume and mean size of *** addition,the probiotic also attenuated the clinical signs of intestinal inflammation inducing a decrease in intestinal and tumor levels of IL-6,TNF-α,IL-17,IL-23 and IL-1β.CONCLUSION Our results suggest a potential chemopreventive effect of probiotic on *** regulates the inflammatory response and preventing CAC.

关键词： Lactobacillus bulgaricus colitis-associated cancer Colorectal cancer Carcinogenesis Probiotics Inflammation

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Roles of phosphatidylinositol-3-kinases signaling pathway in inflammation-related cancer:Impact of rs10889677 variant and buparlisib in colitis-associated cancer

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World Journal of Gastroenterology 2023年第40期29卷 5543-5556页

作者： Nurul Nadirah Razali Raja Affendi Raja Ali Khairul Najmi Muhammad Nawawi Azyani Yahaya Norshafila Diana Mohd Rathi Norfilza Mohd Mokhtar Department of Physiology Faculty of MedicineUniversiti Kebangsaan MalaysiaCheras 56000Kuala LumpurMalaysia School of Medical and Life Sciences Sunway UniversitySunway City 47500Malaysia GUT Research Group Faculty of MedicineUniversiti Kebangsaan MalaysiaCheras 56000Kuala LumpurMalaysia Gastroenterology Unit Department of MedicineFaculty of MedicineUniversiti Kebangsaan MalaysiaCheras 56000Kuala LumpurMalaysia Department of Pathology Faculty of MedicineUniversiti Kebangsaan MalaysiaCheras 56000Kuala LumpurMalaysia

BACKGROUND Phosphatidylinositol-3-kinases(PI3K)is a well-known route in inflammationrelated *** discovery on PI3K-related genes revealed a potential variant that links ulcerative colitis(UC)and colorectal cancer(CRC)with colitisassociated cancer(CAC).PI3K/AKT pathway has been recommended as a potential additional therapeutic option for CRC due to its substantial role in modifying cellular *** is a pan-class I PI3K inhibitor previously shown to reduce tumor *** To investigate the regulation of rs10889677 and the role of buparlisib in the PI3K signaling pathway in CAC *** Genomic DNA from 32 colonic samples,including CAC(n=7),UC(n=10)and CRC(n=15),was sequenced for the rs10889677 *** mutant and wildtype fragments were amplified and cloned in the pmirGLO *** luciferase activity of cloned vectors was assessed after transfection into the HT29 cell *** mice were induced by a mixture of a single azoxymethane injection and three cycles of dextran sulphate sodium,then buparlisib was administered after 14 *** excised colon was subjected to immunohistochemistry for Ki67 and Cleaved-caspase-3 markers and quantitative real-time polymerase chain reaction analysis for Pdk1 and *** Luciferase activity decreased by 2.07-fold in the rs10889677 mutant,confirming the hypothesis that the variant disrupted miRNA binding sites,which led to an increase in IL23R expression and the activation of the PI3K signaling ***,CAC-induced mice had a significantly higher disease activity index(P<0.05).Buparlisib treatment significantly decreased mean weight loss in CAC-induced mice(P<0.05),reduced the percentage of proliferating cells by 5%,and increased the number of apoptotic *** treatment also caused a downward trend of Pdk1 expression and significantly decreased Sgk2 *** Our findings suggested that the rs10889677 variant as a critical initiator of the PI3K signaling pathway,an

关键词： colitis-associated cancer Colorectal cancer Phosphatidylinositol 3-kinase Animal model Luciferases Renilla Phosphatidylinositol 3-kinase inhibitor

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Interleukin-34 deficiency aggravates development of colitis and colitis-associated cancer in mice

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World Journal of Gastroenterology 2022年第47期28卷 6752-6768页

作者： Zhao-Xiu Liu Wei-Jie Chen Yang Wang Bing-Qian Chen Yi-Cun Liu Tiao-Chun Cheng Lei-Lei Luo Lin Chen Lin-Ling Ju Yuan Liu Ming Li Nan Feng Jian-Guo Shao Zhao-Lian Bian Department of Gastroenterology and Hepatology Affiliated Hospital of Nantong UniversityNantong 226001Jiangsu ProvinceChina Medical School Nantong UniversityNantong 226001Jiangsu ProvinceChina Department of Gastroenterology and Hepatology Nantong Third People’s HospitalAffiliated Nantong Hospital 3 of Nantong UniversityNantong 226006Jiangsu ProvinceChina Nantong Institute of Liver Diseases Nantong Third People’s HospitalAffiliated Nantong Hospital 3 of Nantong UniversityNantong 226006Jiangsu ProvinceChina Department of Gastroenterology and Hepatology The Sixth People’s Hospital Affiliated to Shanghai Jiaotong UniversityShanghai 200233China Department of Traditional Chinese Medicine Nantong Third People’s HospitalAffiliated Nantong Hospital 3 of Nantong UniversityNantong 226006Jiangsu ProvinceChina Division of Emergency Ren Ji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai 200120China

BACKGROUND Although expression of interleukin(IL)-34 is upregulated in active ulcerative colitis(UC),the molecular function and underlying mechanism are largely *** To investigate the function of IL-34 in acute colitis,in a wound healing model and in colitis-associated cancer in IL-34-deficient *** colitis was induced by administration of dextran sodium sulfate(DSS),and carcinogenesis was induced by azoxymethane(AOM).Whether the impact of IL-34 on colitis was dependent on macrophages was validated by depletion of macrophages in a murine *** association between IL-34 expression and epithelial proliferation was studied in patients with active *** IL-34 deficiency aggravated murine colitis in acute colitis and in wound healing *** effect of IL-34 on experimental colitis was not dependent on macrophage differentiation and ***-34-deficient mice developed more tumors than wild-type mice following administration of AOM and *** significant difference was shown in degree of cellular differentiation in tumors between wild-type and IL-34-deficient ***-34 was dramatically increased in the active UC patients as previously *** importantly,expression of IL-34 was positively correlated with epithelial cell proliferation in patients with *** IL-34 deficiency exacerbates colonic inflammation and accelerates colitis-associated carcinogenesis in *** might be served as a potential therapeutic target in UC.

关键词： Interleukin-34 Ulcerative colitis Mucosal healing colitis-associated cancer Macrophage Murine model

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Therapy effects of anti-S100a9 antibody on mouse models of colitis and colitis-associated cancer

Therapy effects of anti-S100a9 antibody on mouse models of c...

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第十二届全国免疫学学术大会

作者： Ma Jian Zhang Xuemei Central South University

We previously discovered that the inflammatory factor S100a9 was upregulated dramatically throughout the "inflammation-dysplasia-carcinoma" sequence of colitis-associated cancer(CAC) by means of an azoxymethane(AOM) with dextran sodium sulfate(DSS) induced mouse *** high levels of S100 A9 were observed in clinic colorectal cancer *** investigate the effect of anti-S100a9 antibody on colitis,DSS-treated mice were treated with negative control IgG or anti-S100a9 Ab,as well as anti-TNF-α antibody(infliximab,here used as a positive control).We found that anti-S100a9 Ab or anti-TNF-α Ab significantly ameliorated body weight loss,colon shortening and DAI(disease activity index) ***-S100a9 had modulated cell proliferation,apoptosis,and led to a profound decrease of cytokines such as S100a9,TNF-α,IL-1β,IL-6,IL-17 a,IFN-γ,IL-4 and IL-12 ***-S100a9 Ab also reduced recruitment of macrophages,DCs and *** investigate the effect of anti-S100a9 Ab on colitis-associated cancer,AOM-DSS-induced mouse model was *** found that anti-S100a9 Ab significantly ameliorated DAI scores and colon shortening;reduced tumor incidence and tumor numbers in the CAC model,as compared to those of IgG-treated ***-S100a9 Ab treatment mice showed dramatic reduction of macrophages(CD68) and neutrophils(MPO) in the *** that upregulated in AOM/DSS-induced CAC mice while repressed by anti-S100a9 Ab treatment are mainly involved in cellsubstrate adhesion,Wnt signaling pathway,blood vessel development,inflammatory response,cell proliferation,*** representative molecules(such as P-catenin,p-AKT,CXCL5,p-Smad2) of these key pathways in intestinal tissue were verified by immunohistochemistry *** conclusion,anti-S100a9 Ab ameliorates acute DSS-induced experimental colitis and suppresses AOM/DSS-induced colitis associated cancer in mice,which might be related to the reduction of inflammation cells and cytokines in the ***-S100 ab Ab has

关键词： ulcerative colitis colitis-associated cancer S100a9 Wnt signaling PI3K/AKT signaling TGF-beta

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Contribution of TLR signaling to the pathogenesis of colitisassociated cancer in inflammatory bowel disease

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World Journal of Gastroenterology 2014年第36期20卷 12713-12721页

作者： Ferenc Sipos István Fri Miklós Constantinovits Zsolt Tulassay Gyrgyi Mzes 2nd Department of Internal Medicine Semmelweis University 1088 Budapest Hungary Molecular Medicine Research Unit Hungarian Academy of Sciences 1088 Budapest Hungary

In the intestine a balance between proinflammatory and repair signals of the immune system is essential for the maintenance of intestinal homeostasis. The innate immunity ensures a primary host response to microbial invasion, which induces an inflammatory process to localize the infection and prevent systemic dissemination of pathogens. The key elements of this process are the germline encoded pattern recognition receptors including Toll-like receptors (TLRs). If pathogens cannot be eliminated, they may elicit chronic inflammation, which may be partly mediated via TLRs. Additionally, chronic inflammation has long been suggested to trigger tissue tumorous transformation. Inflammation, the seventh hallmark of cancer, may affect all phases of tumor development, and evade the immune system. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability. Furthermore, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Colorectal cancers in inflammatory bowel disease patients are considered typical examples of inflammation-related cancers. Although data regarding the role of TLRs in the pathomechanism of cancer-associated colitis are rather conflicting, functionally these molecules can be classified as ”largely antitumorigenic” and ”largely pro-tumorigenic” with the caveat that the underlying signaling pathways are mainly context (i.e., organ-, tissue-, cell-) and ligand-dependent.

关键词： Inflammation Tissue repair Immunoregulation colitis-associated cancer Toll-like receptor Inflammatory bowel disease Carcinogenesis

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Inflammatory bowel disease-related colorectal cancer:Past,present and future perspectives

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World Journal of Gastrointestinal Oncology 2022年第3期14卷 547-567页

作者： Snehali Majumder Uday Nagesh Shivaji Rangarajan Kasturi Alben Sigamani Subrata Ghosh Marietta Iacucci Department of Clinical Research Narayana HealthBangalore 560099KarnatakaIndia National Institute for Health Research Birmingham Biomedical Research Centre University Hospitals BirminghamBirmingham B152THUnited Kingdom Institute of Immunology and Immunotherapy University of BirminghamBirmingham B152THUnited Kingdom Department of Gastroenterology Narayana HealthBangalore 560099India

Inflammatory bowel disease-related colorectal cancer(IBD-CRC)is one of the most serious complications of IBD contributing to significant mortality in this cohort of *** is often associated with diet and lifestyle-related gut microbial dysbiosis,the interaction of genetic and environmental factors,leading to chronic gut *** to the“common ground hypothesis”,microbial dysbiosis and intestinal barrier impairment are at the core of the chronic inflammatory process associated with *** the many underlying factors known to increase the risk of IBD-CRC,perhaps the most important factor is chronic persistent *** persistent inflammation in the colon results in increased proliferation of cells necessary for repair but this also increases the risk of dysplastic changes due to chromosomal and microsatellite *** pathways have been identified,regulated by many positive and negative factors involved in the development of cancer,which in this case follows the‘inflammation-dysplasia-carcinoma’*** to lower this risk are extremely important to reduce morbidity and mortality due to IBD-CRC,among which colonoscopic surveillance is the most widely accepted and implemented modality,forming part of many national and international ***,the effectiveness of surveillance in IBD has been a topic of much debate in recent years for multiple reasons—cost-benefit to health systems,resource requirements,and also because of studies showing conflicting long-term *** review provides a comprehensive overview of past,present,and future perspectives of *** explore and analyse evidence from studies over decades and current best practices followed *** the future directions section,we cover emerging novel endoscopic techniques and artificial intelligence that could play an important role in managing the risk of IBD-CRC.

关键词： Inflammatory bowel disease Colorectal cancer colitis-associated cancer Surveillance in inflammatory bowel disease Dye-spray colonoscopy Adenomas Dysplasia Colectomy

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Myo-inositol reduces β-catenin activation in colitis

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World Journal of Gastroenterology 2017年第28期23卷 5115-5126页

作者： Emily M Bradford Corey A Thompson Tatiana Goretsky Guang-Yu Yang Luz M Rodriguez Linheng Li Terrence A Barrett Division of Gastroenterology Department of Internal MedicineUniversity of Kentucky Department of Internal Medicine Northwestern University Feinberg School of Medicine Division of cancer Research National Cancer InstituteDCP/GOCRGBethesda Department of Surgery Walter Reed National Military Medical Center Department of Pathology and Laboratory Medicine University of Kansas School of Medicine and Stowers Institute for Medical Research

To assess dietary myo-inositol in reducing stem cell activation in colitis, and validate pβ-cateninS552 as a biomarker of recurrent *** examined the effects of dietary myo-inositol treatment on inflammation, pβ-cateninS552 and pAkt levels by histology and western blot in IL-10-/- and dextran sodium sulfate-treated colitic mice. Additionally, we assessed nuclear pβ-cateninS552 in patients treated with myo-inositol in a clinical trial, and in patients with and without a history of colitis-induced *** mice, pβ-cateninS552 staining faithfully reported the effects of myo-inositol in reducing inflammation and intestinal stem cell activation. In a pilot clinical trial of myo-inositol administration in patients with a history of low grade dysplasia (LGD), two patients had reduced numbers of intestinal stem cell activation compared to the placebo control patient. In humans, pβ-cateninS552 staining discriminated ulcerative colitis patients with a history of LGD from those with benign *** crypts with increased numbers of pβ-cateninS552 - positive cells can be utilized as a biomarker in colitis-associated cancer chemoprevention trials.

关键词： Chemoprevention Dysplasia Biomarker Stem cell colitis-associated cancer

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Hepatocyte nuclear factor 4-alpha involvement in liver and intestinal inflammatory networks

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World Journal of Gastroenterology 2014年第1期20卷 22-30页

作者： Jean-Philippe Babeu Franois Boudreau Département d’ Anatomie et de Biologie Cellulaire Faculté de Médecine et des Sciences de la SantéUniversité de SherbrookeSherbrooke J1E 4K8QuébecCanada

Hepatocyte nuclear factor 4-alpha (HNF4-α) is a nuclear receptor regulating metabolism, cell junctions, differentiation and proliferation in liver and intestinal epithelial cells. Mutations within the HNF4A gene are associated with human diseases such as maturity-onset diabetes of the young. Recently, HNF4A has also been described as a susceptibility gene for ulcerative colitis in genome-wide association studies. In addition, specific HNF4A genetic variants have been identified in pediatric cohorts of Crohn’s disease. Results obtained from knockout mice supported that HNF4-α can protect the intestinal mucosae against inflammation. However, the exact molecular links behind HNF4-α and inflammatory bowel diseases remains elusive. In this review, we will summarize the current knowledge about the role of HNF4-α and its isoforms in inflammation. Specific nature of HNF4-α P1 and P2 classes of isoforms will be summarized. HNF4-α role as a hepatocyte mediator for cytokines relays during liver inflammation will be integrated based on documented examples of the literature. Conclusions that can be made from these earlier liver studies will serve as a basis to extrapolate correlations and divergences applicable to intestinal inflammation. Finally, potential functional roles for HNF4-α isoforms in protecting the intestinal mucosae from chronic and pathological inflammation will be presented.

关键词： Hepatocyte nuclear factor 4-alpha Inflammatory bowel diseases colitis-associated cancer Gastrointestinal tract Intestinal epithelium barrier Inflammation

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