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Polymorphisms of the TLR2 and TLR4 genes are associated with risk of gastric cancer in a Brazilian population

World Journal of Gastroenterology 2012年第11期18卷 1235-1242页

作者： Juliana Garcia de Oliveira ana elizabete silva Department of Biology UNESP-So Paulo State UniversitySo José do Rio Preto Campus15054-000 SPBrazil

AIM： TO investigate toll-like receptor 2 （TLR2） -196 to -274 del, and TLR4 （＋896A/G rs4986790 and ＋1196C/ T rs4986791） polymorphisms at risk of chronic gastritis and gastric cancer in a Brazilian population and associ-ation of gastric lesions with risk factors such as smoking, alcohol intake and Helicobacter pylori infection.METHODS： In this casecontrol study, polymorphism at TLR2 -96 to -174 del was investigated by using the allele-specific polymerase chain reaction （PCR） method, while the PCR-restriction fragment length polymorphism technique was carried out to identify the TLR4 （rs4986790 and rs4986791） genotypes in 607 Brazilian individuals （208 with chronic gastritis-CG, 174 with gastric cancer-GC and 225 controls -C）.RESULTS： The single nucleotide polymorphisms TLR4＋1196ClT was not associated with risk of chronic gastritis or gastric cancer and the homozygous genotypes TLR4＋896GG and TLR4＋1196TF were absent in the studied population. However, the frequency of TLR2 -196 to -174 ins/del ＋ del/del and TLR4＋896AGgenotypes was significantly higher （P 〈 0.01 and P = 0.01, respectively） in the cancer group （33.4% and 11.5%, respectively） than in the control group （16.9% and 4.5%, respectively）. It was also observed that the G-C haplotype of the TLR4＋896A/G＋1196C/T （P = 0.02） and the combination of variant alleles of the TLR21TLR4＋896G （P = 0.02） are associated with susceptibility to gastric cancer. In addition, the multiple logistic regression showed that male gender [odds ratio （OR） = 2.70; 95% CI： 1.66-4.41; P 〈 0.01], alcohol intake （OR = 2.93; 95% CI： 1.76-4.87, P 〈 0.01）, TLR2 -196 to -174 del （OR = 2.64; 95% CI： 1.56-4.44; P 〈 0.01） and TLR4＋896G （OR = 3.19; 95% CI： 1.34- 7.61; P 〈 0.01） polymorphisms were associated with a higher susceptibility to developing this neoplasm.CONCLUSION： Our data indicate that T/R2 -196 to -174 del and TLR4＋896G may increase the risk of gastric cancer in a Brazilian population.

关键词： Polymorphisms Toll-like receptor 2 Toll-like receptor 4 Gastric cancer Gastritis

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Up-regulation of tumor necrosis factor-a pathway survival genes and of the receptor TNFR2 in gastric cancer

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World Journal of Gastrointestinal Oncology 2019年第4期11卷 281-294页

作者： ana Flavia Teixeira Rossi Julia Cocenzo Contiero Fernanda da silva Manoel-Caetano Fabio Eduardo Severino ana elizabete silva Department of Biology Sao Paulo State University–UNESP Department of Surgery and Orthopedics Faculty of Medicine Sao Paulo State University–UNESP

BACKGROUND Gastric carcinogenesis can be induced by chronic inflammation triggered by Helicobacter pylori(H. pylori) infection. Tumor necrosis factor(TNF)-α and its receptors(TNFR1 and TNFR2) regulate important cellular processes, such as apoptosis and cell survival, and the disruption of which can lead to cancer. This signaling pathway is also modulated by microRNAs(miRNAs), altering gene *** To evaluate the mRNA and miRNAs expression involved in the TNF-α signaling pathway in gastric cancer(GC) tissues and its *** Quantitative polymerase chain reaction(qPCR) by TaqMan? assay was used to quantify the RNA transcript levels of TNF-α signaling pathway(TNF, TNFR1,TNFR2, TRADD, TRAF2, CFLIP, NFKB1, NFKB2, CASP8, CASP3) and miRNAs that targets genes from this pathway(miR-19 a, miR-34 a, miR-103 a, miR-130 a,miR-181 c) in 30 GC fresh tissue samples. Molecular diagnosis of H. pylori was performed by nested PCR for gene HSP60. A miRNA:mRNA interaction network was construct using Cytoscape v3.1.1 from the in silico analysis performed using public *** Up-regulation of cellular survival genes as TNF, TNFR2, TRADD, TRAF2, CFLIP,and NFKB2, besides CASP8 and miR-34 a was observed in GC tissues, whereas mediators of apoptosis such as TNFR1 and CASP3 were down-regulated. When the samples were stratified by histological type, the expression of miR-103 a and miR-130 a was significantly increased in the diffuse-type of GC compared to the intestinal-type. However, no influence of H. pylori infection was observed on the expression levels of mRNA and miRNAs analyzed. Moreover, the miRNA:mRNA interaction network showed several interrelations between the miRNAs and their target genes, highlighting miR-19 a and miR-103 a, which has as predicted or validated target a large number of genes in the TNF-α pathway,including TNF, TNFR1, TNFR2, CFLIP, TRADD, CASP3 and *** Our findings show that cell survival genes mediated by TNF/TNFR2 binding

关键词： Gastric cancer Tumor necrosis factor-a signaling TNFR1 TNFR2 Cellular survival MicroRNAs

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Helicobacter pylori infection: Host immune response, implications on gene expression and microRNAs

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World Journal of Gastroenterology 2014年第6期20卷 1424-1437页

作者： Aline Cristina Targa Cadamuro ana Flávia Teixeira Rossi Nathália Maciel Maniezzo ana elizabete silva Department of Biology UNESP-So Paulo State University Campus So José do Rio Preto

Helicobacter pylori(H. pylori) infection is the most common bacterial infection worldwide. Persistent infection of the gastric mucosa leads to inflammatory processes and may remain silent for decades or progress causing more severe diseases, such as gastric adenocarcinoma. The clinical consequences of H. pylori infection are determined by multiple factors, including host genetic predisposition, gene regulation, environmental factors and heterogeneity of H. pylori virulence factors. After decades of studies of this successful relationship between pathogen and human host, various mechanisms have been elucidated. In this review, we have made an introduction on H. pylori infection and its virulence factors, and focused mainly on modulation of host immune response triggered by bacteria, changes in the pattern of gene expression in H. pylori-infected gastric mucosa, with activation of gene transcription involved in defense mechanisms, inflammatory and immunological response, cell proliferation and apoptosis. We also highlighted the role of bacteria eradication on gene expression levels. In addition, we addressed the recent involvement of different microRNAs in precancerous lesions, gastric cancer, and inflammatory processes induced by bacteria. New discoveries in this field may allow a better understanding of the role of major factors involved in the pathogenic mechanisms of H. pylori.

关键词： Helicobacter pylori Inflammation Virulence factors Immune response Gastric lesions Gastric cancer Gene expression MicroRNAs

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GSTT1,GSTM1 and CYP2E1 genetic polymorphisms in gastric cancer and chronic gastritis in a Brazilian population

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World Journal of Gastroenterology 2004年第9期10卷 1240-1245页

作者： Jucimara Colombo ana elizabete silva Andréa Regina Baptista Rossit Alaor Caetano Aldenis Albaneze Borim Durval Wohnrath Departamento de Biologia UNESP-Campus de So José do Rio Preto-SPBrazil Departamento de Doencas Dermatológicas Infecciosas e ParasitáriasFaculdade de MedicinaFAMERPSo José do Rio PretoSPBrazil Hospital de Base Faculdade de MedicinaFAMERE So José do Rio PretoSPBrazil Fundaco Pio Ⅻ BarretosBrazil

AIM:To test the hypothesis that,in the Southeastern Brazilian population,the GSTT1,GSTM1 and CYP2E1 polymorphisms and putative risk factors are associated with an increased risk for gastric cancer. METHODS:We conducted a study on 100 cases of gastric cancer (GC),100 cases of chronic gastritis (CG),and 150 controls (C).Deletion of the GSTT1 and GSTM1 genes was assessed by multiplex ***2E1/Pst1 genotyping was performed using a PCR-RFLP assay. RESULTS:No relationship between GSTT1/GSTM1 deletion and the c1/c2 genotype of CYP2E1 was observed among the three ***,a significant difference between CG and C was observed,due to a greater number of GSTT1/GSTM1 positive genotypes in the CG *** GSTT1 null genotype occurred more frequently in Negroid subjects,and the GSTM1 null genotype in Caucasians,while the GSTM1 positive genotype was observed mainly in individuals with chronic gastritis infected with H pylori. CONCLUSION:Our findings indicate that there is no obvious relationship between the GSTT1,GSTM1 and CYP2E1 polymorphisms and gastric cancer.

关键词： Polymorphism, Genetic Adolescent Adult Aged Aged, 80 and over Brazil Case-Control Studies Chronic Disease Cytochrome P-450 CYP2E1 Female Gastritis Genotype Glutathione Transferase Humans Male Middle Aged Research Support, Non-U.S. Gov't Risk Factors Stomach Neoplasms

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Downregulation of TNFR2 decreases survival gene expression,promotes apoptosis and affects the cell cycle of gastric cancer cells

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World Journal of Gastroenterology 2022年第24期28卷 2689-2704页

作者： ana Flávia Teixeira Rossi Fernanda da silva Manoel-Caetano Joice Matos Biselli Ágata silva Cabral Marilia de Freitas Calmon Saiki Marcelo Lima Ribeiro ana elizabete silva Department of Biological Sciences Sao Paulo State University(UNESP)São Josédo Rio Preto 15054-000São PauloBrazil Clinical Pharmacology and Gastroenterology Unit São Francisco University(USF)Bragança Paulista 12916-900São PauloBrazil

BACKGROUND Chronic inflammation due to Helicobacter pylori(***)infection promotes gastric *** necrosis factor-α(TNF-α),a key mediator of inflammation,induces cell survival or apoptosis by binding to two receptors(TNFR1 and TNFR2).TNFR1 can induce both survival and apoptosis,while TNFR2 results only in cell *** dysregulation of these processes may contribute to *** To evaluate the effects of TNFR1 and TNFR2 downregulation in AGS cells treated with *** extract on the TNF-α*** AGS cell lines containing TNFR1 and TNFR2 receptors downregulated by specific shRNAs and nonsilenced AGS cells were treated with *** extract for 6 ***,quantitative polymerase chain reaction with TaqMan®assays was used for the relative quantification of the mRNAs(TNFA,TNFR1,TNFR2,TRADD,TRAF2,CFLIP,NFKB1,NFKB2,CASP8,CASP3)and miRNAs(miR-19a,miR-34a,miR-103a,miR-130a,miR-181c)related to the TNF-αsignalling *** cytometry was employed for cell cycle analysis and apoptosis *** In nonsilenced AGS cells,*** extract treatment increased the expression of genes involved in cell survival and inhibited both apoptosis(NFKB1,NFKB2 and CFLIP)and the TNFR1 ***1 downregulation significantly decreased the expression of the TRADD and CFLIP genes,although no change was observed in the cellular process or miRNA *** contrast,TNFR2 downregulation decreased the expression of the TRADD and TRAF2 genes,which are both important downstream mediators of the TNFR1-mediated pathway,as well as that of the NFKB1 and CFLIP genes,while upregulating the expression of miR-19a and ***,a reduction in the number of cells in the G0/G1 phase and an increase in the number of cells in the S phase were observed,as well as the promotion of early *** Our findings mainly highlight the important role of TNFR2 in the TNF-αpathway in gastric cancer,indicating that silencing it can reduce the

关键词： Gastric cancer Helicobacter pylori Tumour necrosis factor-αsignalling pathway TNFR1 TNFR2 miRNAs

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Upregulation of the APE1 and H2AX genes and miRNAs involved in DNA damage response and repair in gastric cancer

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Genes & Diseases 2019年第2期6卷 176-184页

作者： Fernanda S.Manoel-Caetano ana Flávia T.Rossi Gabriela Calvet de Morais Fábio Eduardo Severino ana elizabete silva Department of Biology UNESPSāo Paulo State UniversityCampus of Sāo Josédo Rio PretoRua Cristòvāo Colombo226515.054-000Sāo Josédo Rio PretoSāo PauloBrazil Department of Surgery and Orthopedics Faculty of MedicineUNESPSāo Paulo State UniversityCampus of BotucatuAv.Prof.Mário Rubens Guimarāes Montenegros/n18.618-687BotucatuSāo PauloBrazil

Gastric cancer remains one of the leading causes of cancer-related death worldwide,and most of the cases are associated with Helicobacter pylori *** bacterium promotes the production of reactive oxygen species(ROS),which cause DNA damage in gastric epithelial *** this study,we evaluated the expression of important genes involved in the recognition of DNA damage(ATM,ATR,and H2AX)and ROS-induced damage repair(APE1)and the expression of some miRNAs(miR-15a,miR-21,miR-24,miR-421 and miR-605)that target genes involved in the DNA damage response(DDR)in 31 fresh tissues of gastric *** v3.1.1 was used to construct the postulated miRNA:mRNA interaction *** performed by real-time quantitative PCR exhibited significantly increased levels of the APE1(RQ=2.55,panalysis reinforced some of the gene:gene(ATM/ATR/H2AX)and miRNA:mRNA relationships obtained also with the interaction ***,our findings show that tumor cells from gastric cancer presents deregulation of genes and miRNAs that participate in the recognition and repair of DNA damage,which could confer an advantage to cell survival and proliferation in the tumor microenvironment.

关键词： DNA damage response DNA repair Gastric cancer Gene expression microRNA

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Polymorphisms of DNA repair genes XRCC1 and XRCC3, interaction with environmental exposure and risk of chronic gastritis and gastric cancer

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World Journal of Gastroenterology 2005年第42期11卷 6593-6600页

作者： Márcia Cristina Duarte Jucimara Colombo Andrea Regina Baptista Rossit Alaor Caetano Aldenis Albaneze Borim Durval Wornrath ana elizabete silva UNESP-S(a|~)o Paulo State University Department of Biology Campus S(a|~)o José do Rio Preto SP Brazil FAMERP- S(a|~)o José do Rio Preto School of Medicine Microorganism Investigation Center S(a|~)o José do Rio Preto SP Brazil FAMERP-S(a|~)o José do Rio Preto School of Medicine Hospital de Base S(a|~)o José do Rio Preto SP Brazil Pio Ⅻ Foundation Barretos SP Brazil UNESP- S(a|~)o Paulo State University Department of Biology Campus S(a|~)o José do Rio Preto SP Brazil

AIM： TO evaluate the association between poly- morphisms XRCC1 Arg194Trp and Arg399GIn and XRCC3 Thr241Met and the risk for chronic gastritis and gastric cancer, in a Southeastern Brazilian population. METHODS： Genotyping by PCR-RFLP was carried out on 202 patients with chronic gastritis （CG） and 160 patients with gastric cancer （GC）, matched to 202 （Cl） and 150 （C2） controls, respectively. RESULTS： No differences were observed among the studied groups with regard to the genotype distribution of XRCC1 codons 194 and 399 and of XRCC3 codon 241. However, the combined analyses of the three variant alleles （194Trp, 399Gin and 241Met） showed an increased risk for chronic gastritis when compared to the GC group. Moreover, an interaction between the polymorphic alleles and demographic and environmental factors was observed in the CG and GC groups. XRCC1 194Trp was associated with smoking in the CG group, while the variant alleles XRCC1 399Gin and XRCC3 241Met were related with gender, smoking, drinking and Hpylori infection in the CG and GC groups. CONCLUSION： Our results showed no evidence of a rela-tionship between the polymorphisms XRCC1 Arg194Trp and Arg399Gln and XRCC3 Thr241Met and the risk of chronic gastritis and gastric cancer in the Brazilianpopulation, but the combined effect of these variants may interact to increase the risk for chronic gastritis, considered a premalignant lesion. Our data also indicate a gene-environment interaction in the susceptibility to chronic gastritis and gastric cancer.

关键词： Gastric cancer Gastritis XRCC1 XRCC3 Polymorphism Environmental exposure

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Toll-like receptor 9 polymorphisms and Helicobacter pylori influence gene expression and risk of gastric carcinogenesis in the Brazilian population

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World Journal of Gastrointestinal Oncology 2019年第11期11卷 998-1010页

作者： Manoela Dias Susi de Matos Lourenco Caroline Lucas Trevizani Rasmussen Spencer Luis Marques Payao ana Flavia Teixeira Rossi ana elizabete silva Juliana Garcia de Oliveira-Cucolo Department of Graduate-Level Research USCSacred Heart UniversityBauru 17011-970SPBrazil Department of Genetics and Molecular Biology FAMEMA-Marilia Medical SchoolMarília 17519-030SPBrazil Department of Biology Sao Paulo State University-UNESPSao Jose do Rio Preto 15054-000SPBrazil Department of Molecular Biological and Genetics and Molecular Biology Research Unit-UPGEMFaculty of Medicine of Sao Jose do Rio Preto-FAMERPSao Jose do Rio Preto 15090-000SPBrazil

BACKGROUND Toll-like receptors(TLRs)are the first line of host defense,and are involved in Helicobacter pylori(***)recognition and activation of both inflammatory and carcinogenic *** presence of single nucleotide polymorphisms(SNPs)in genes that activate the immune response may modulate the risk of precancerous lesions and gastric cancer(GC).Among them,Toll-like receptor 9(TLR9)polymorphisms have emerged with a risk factor of infectious diseases and cancer,however the studies are still *** To evaluate whether TLR9 rs5743836 and rs187084 SNPs contribute to the risk of gastric carcinogenesis,and its influence on mRNA *** A case-control study was conducted to evaluate two TLR9 SNPs(TLR9-1237 TCrs5743836 and TLR9-1486 CT-rs187084)in chronic gastritis(CG)and GC patients.A total of 609 DNA samples of peripheral blood[248 CG,161 GC,and 200 samples from healthy individuals(C)]were genotyped by polymerase chain reaction-restriction fragment length *** samples were tested for the *** infection using Hpx1 and Hpx2 *** polymerase chain reaction by TaqMan?assay was used to quantify TLR9 mRNA from fresh gastric tissues(48 GC,26 CG,and 14 C).RESULTS For TLR9-1237,the TC+CC or CC genotypes were associated with a higher risk of GC than C[recessive model odds ratio(OR)=5.01,95%confidence interval(CI):2.52-9.94,P<0.0001],and the CG(recessive model OR=4.63;95%CI:2.44-8.79,P<0.0001)*** TLR9-1486,an association between the CT+TT genotypes and increased risk of both GC(dominant model OR=2.72,95%CI:1.57-4.72,P<0.0001)and CG(dominant model OR=1.79,95%CI:1.15-2.79,P=0.0094)was observed when compared to the C ***,the presence of TLR9-1237 TC/CC+TLR9-1486 CC genotypes potentiate the risk for this neoplasm(OR=18.57;95%CI:5.06-68.15,P<0.0001).The TLR9 mRNA level was significantly higher in the GC group(RQ=9.24,P<0.0001)in relation to the CG group(RQ=1.55,P=0.0010)and normal mucosa(RQ=1.0).When the sa

关键词： Toll-like receptor 9 Helicobacter pylori Gastric cancer Chronic gastritis Polymorphisms Gene expression

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TLR2 and TLR4 polymorphisms influence m RNA and protein expression in colorectal cancer

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World Journal of Gastroenterology 2015年第25期21卷 7730-7741页

作者： Marcela Alcantara Proenca Juliana Garcia de Oliveira Aline Cristina Targa Cadamuro Maysa Succi Joao Gomes Netinho Eny Maria Goloni-Bertolo érika Cristina Pavarino ana elizabete silva Department of Biology UNESPSao Paulo State University USC-Sacred Heart University PróReitoria de Pesquisa e Pós Graduacao Department of Surgery School of MedicineFAMERPSao Josédo Rio Preto 15090-000SPBrazil UPGEM School of MedicineFAMERPSao Josédo Rio Preto 15090-000SPBrazil

AIM: To evaluate the effect of promoter region polymorphisms of toll-like receptor(TLR)2-196 to-174 del and TLR4-1607T/C(rs10759932) on m RNA and protein expression in tumor tissue and of TLR4+896A/G(rs4986790) on colorectal cancer(CRC) ***: The TLR2-196 to-174 del polymorphism was investigated using allele-specific polymerase chain reaction(PCR) and the TLR4-1607T/C and TLR4+896A/G by PCR-restriction fragment length p o l y m o r p h i s m( R F L P). W e g e n o t y p e d 4 3 4 D N A samples from 194 CRC patients and 240 healthy individuals. The m RNA relative quantification(RQ) was performed in 40 tumor tissue samples by quantitative PCR Taq Man assay, using specific probes for TLR2 and TLR4 genes, and ACTB and GAPDH reference geneswere used as endogenous controls. Protein expression was analyzed by immunohistochemistry with specific primary ***: No association was found for TLR4-1607T/C and TLR4+896A/G by three statistical models(logadditive, dominant and recessive). However, based on dominant and log-additive models, the polymorphic variant TLR2-196 to-174 del was associated with increased CRC risk [dominant: odds ratio(OR) = 1.72, 95%CI: 1.03-2.89; P = 0.038 and log-additive: OR =1.59, 95%CI: 1.02-2.48; P = 0.039]. TLR2 m RNA expression was increased in tumor tissue(RQ = 2.36) when compared to adjacent normal tissue(RQ = 1; P analysis of TLR2 and TLR4 protein expression was concordant with the findings of m RNA expression. In addition, the TLR2-196 to-174 del variant carriers showed m RNA relative expression 2.19 times higher than wild-genotype carriers. The TLR2 protein expression was also higher for the TLR2-196 to-174 del variant carriers [117 ± 10 arbitrary unit(a.u.) vs 95 ± 4 a.u., P = 0.03]. However, for the TLR4-1607T/C polymorphism no significant difference was found for both m RNA(P = 0.56) and protein expression(P

关键词： Toll-like receptor 2 Toll-like receptor 4 Colorectal cancer Protein expression Gene expression Genetic polymorphisms

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Relationship between Fusobacterium nucleatum,inflammatory mediators and microRNAs in colorectal carcinogenesis

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World Journal of Gastroenterology 2018年第47期24卷 5351-5365页

作者： Marcela Alcantara Proenca Joice Matos Biselli Maysa Succi Fábio Eduardo Severino Gustavo Noriz Berardinelli Alaor Caetano Rui Manuel Reis David J Hughes ana elizabete silva Department of Biology UNESPUniv. Estadual PaulistaCampus of Sao Jose do Rio PretoSao Jose do Rio PretoSao Paulo 15054-000Brazil Department of Surgery and Orthopedics Faculty of MedicineUNESPUniv. Estadual PaulistaCampus of BotucatuBotucatuSao Paulo 18618-687Brazil Endoscopy Center of Rio Preto Sao Jose do Rio PretoSao Paulo 15015-700Brazil Molecular Oncology Research Center Barretos Cancer HospitalBarretosSao Paulo 14784-400Brazil Life and Health Sciences Research Institute University of MinhoCampus GualtarBraga 4710-057Portugal ICVS/3B’s-PT Government Associate Laboratory Campus GualtarBraga 4710-057Portugal Cancer Biology and Therapeutics Group UCD Conway InstituteUniversity College DublinDublin D04 V1W8Ireland

AIM To examine the effect of Fusobacterium nucleatum(F. nucleatum) on the microenvironment of colonic neoplasms and the expression of inflammatory mediators and microRNAs(miRNAs).METHODS Levels of F. nucleatum DNA, cytokine gene mRNA(TLR2, TLR4, NFKB1, TNF, IL1 B, IL6 and IL8), and potentially interacting miRNAs(miR-21-3p, miR-22-3p, mi R-28-5p, miR-34a-5p, miR-135b-5p) were measured by quantitative polymerase chain reaction(qPCR) TaqMan? assays in DNA and/or RNA extracted from the disease and adjacent normal fresh tissues of 27 colorectal adenoma(CRA) and 43 colorectal cancer(CRC) patients. KRAS mutations were detected by direct sequencing and microsatellite instability(MSI) status by multiplex PCR. Cytoscape v3.1.1 was used to construct the postulated miRNA:mRNA interaction *** Overabundance of F. nucleatum in neoplastic tissue compared to matched normal tissue was detected in CRA(51.8%) and more markedly in CRC(72.1%). We observed significantly greater expression of TLR4, IL1 B, IL8, and miR-135 b in CRA lesions and TLR2, IL1 B, IL6, IL8, mi R-34 a and miR-135 b in CRC tumours compared to their respective normal tissues. Only two transcripts for miR-22 and miR-28 were exclusively downregulated in CRC tumour samples. The mRNA expression of IL1 B, IL6, IL8 and miR-22 was positively correlated with F. nucleatum quantification in CRC tumours. The mRNA expression of miR-135 b and TNF was inversely correlated. The miRNA:mRNA interaction network suggested that the upregulation of miR-34 a in CRC proceeds via a TLR2/TLR4-dependent response to F. nucleatum. Finally, KRAS mutations were more frequently observed in CRC samples infected with F. nucleatum and were associated with greater expression of miR-21 in CRA, while IL8 was upregulated in MSI-high *** Our findings indicate that F. nucleatum is a risk factor for CRC by increasing the expression of inflammatory mediators through a possible mi RNA-mediated activation of TLR2/TLR4.

关键词： Colorectal cancer Colorectal adenoma Fusobacterium nucleatum Inflammation Cytokines MicroRNAs

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