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

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

作者： Marcela Alcantara Proenca joice matos.bis.lli 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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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.bis.lli 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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