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Decreased expression of microRNA-629 in gastric cancer samples potentiated by the virulence marker of H. pylori, cagA gene

dc.contributor.authorSoares, Caroline Dos Reis Rodrigues
dc.contributor.authorDa Silva, Lucas Matheus Vieira
dc.contributor.authorAlmeida, Bianca Reis
dc.contributor.authorPereira, Jéssica Nunes [UNESP]
dc.contributor.authorSantos, Mônica Pezenatto Dos
dc.contributor.authorBarbosa, Mônica Santiago
dc.contributor.authorSmith, Marília De Arruda Cardoso
dc.contributor.authorPayão, Spencer Luiz Marques
dc.contributor.authorRasmussen, Lucas Trevizani
dc.contributor.institutionFaculdade de Medicina de Marília
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Federal de Goiás (UFG)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionCentro Universitário das Faculdades Integradas de Ourinhos
dc.date.accessioned2025-04-29T18:56:56Z
dc.date.issued2024-01-01
dc.description.abstractBackground – Helicobacter pylori (H. pylori) is a gram-negative bacterium associated with the etiology of several gastrointestinal tract pathologies, and cagA-positive (cagA+) strains are found in populations with gastric ulcers and precancerous lesions, inducing pro-inflammatory responses. The development of neoplasms is related to microRNA (miRNA) dysregulation, indicating highly expressed miRNA-629. The article aims to correlate the expression level of miRNA-629 with the presence of H. pylori and the pathogenicity marker cagA. Methods – 203 gastric biopsy samples were evaluated from individuals with normal gastric tissue (n=60), gastritis (n=96), and gastric cancer (n=47) of both genders and over 18 years old. The samples were subdivided according to the presence or absence of H. pylori, detected by polymerase chain reaction (PCR). RNA was extracted using a commercial kit and quantified. Complementary DNA (cDNA) was synthesized using commercial kits, and the relative expression was calculated using the 2-ΔΔCt method. Results – Individuals infected with H. pylori are nine times more likely to develop gastric cancer. Cancer patients appeared to have decreased expression of miRNA-629; however, the presence of the bacterium would not influence this reduction. Individuals in the cancer group showed lower miRNA-629 expression when cagA+; however, in the control group, the expression was higher when cagA+. Conclusion – H. pylori is a factor involved in the etiology and progression of gastric diseases. Reduction in miRNA-629 expression in cancer patients occurs independent of the presence of the bacterium, but when the cagA pathogenicity marker is present, it induces changes in the gene expression of the respective miRNA.en
dc.description.affiliationFaculdade de Medicina de Marília, SP
dc.description.affiliationFaculdade de Medicina de Botucatu, SP
dc.description.affiliationUniversidade Estadual de Campinas, SP
dc.description.affiliationUniversidade Federal de Goiás, GO
dc.description.affiliationUniversidade Federal de São Paulo, SP
dc.description.affiliationCentro Universitário das Faculdades Integradas de Ourinhos, SP
dc.description.affiliationUnespFaculdade de Medicina de Botucatu, SP
dc.identifierhttp://dx.doi.org/10.1590/S0004-2803.24612023-139
dc.identifier.citationArquivos de Gastroenterologia, v. 61.
dc.identifier.doi10.1590/S0004-2803.24612023-139
dc.identifier.issn1678-4219
dc.identifier.issn0004-2803
dc.identifier.scopus2-s2.0-85194021530
dc.identifier.urihttps://hdl.handle.net/11449/301005
dc.language.isoeng
dc.language.isopor
dc.relation.ispartofArquivos de Gastroenterologia
dc.sourceScopus
dc.subjectchronic gastritis
dc.subjectgastric diseases
dc.subjectHelicobacter pylori
dc.subjectinflammation
dc.subjectmicroRNA
dc.subjectvirulence factors
dc.titleDecreased expression of microRNA-629 in gastric cancer samples potentiated by the virulence marker of H. pylori, cagA geneen
dc.titleDiminuição da expressão do microRNA-629 em amostras de câncer gástrico potencializada pelo marcador de virulências do H. pylori, gene cagApt
dc.typeArtigopt
dspace.entity.typePublication
relation.isOrgUnitOfPublicationa3cdb24b-db92-40d9-b3af-2eacecf9f2ba
relation.isOrgUnitOfPublication.latestForDiscoverya3cdb24b-db92-40d9-b3af-2eacecf9f2ba
unesp.author.orcid0000-0003-0038-676X[1]
unesp.author.orcid0009-0000-9969-2163[2]
unesp.author.orcid0009-0006-8032-0363[3]
unesp.author.orcid0000-0001-6949-2160[4]
unesp.author.orcid0000-0003-2298-826X[5]
unesp.author.orcid0000-0001-7948-8421[6]
unesp.author.orcid0000-0002-1441-1033[7]
unesp.author.orcid0000-0003-4373-7742[8]
unesp.author.orcid0000-0002-9033-2257[9]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt

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