Expression of miRNA‐146a, miRNA‐155, IL‐2, and TNF‐α in inflammatory response to <i>Helicobacter pylori</i> infection associated with cancer progression

Zabaglia, Luanna Munhoz; Sallas, Mayara Luciana; Santos, Mônica Pezenatto dos; Orcini, Wilson Aparecido; Peruquetti, Rita Luiza; Constantino, Dulce Helena Jardim; Chen, Elizabeth; Smith, Marı́lia de Arruda Cardoso; Payão, Spencer-Luiz Marques; Rasmussen, Lucas Trevizani

doi:10.1111/ahg.12234

Cited by 20 publications

(16 citation statements)

References 34 publications

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“…MiRNAs have no ability to encode proteins, but contribute to the modulation of gene expression[11,12]. A recent study revealed the upregulation of miR-146a and miR-155 in patients with gastritis induced by H. pylori infection[13], with the similar findings demonstrated by another research group[14]. Cortés-Márquez et al[14] further grouped the patients with gastritis by age, and found that both children and adults with H. pylori -induced gastritis displayed higher levels of miR-145a and miR-155.…”

Section: Introductionmentioning

confidence: 99%

“…Cortés-Márquez et al[14] further grouped the patients with gastritis by age, and found that both children and adults with H. pylori -induced gastritis displayed higher levels of miR-145a and miR-155. Moreover, the cancerization tendency of H. pylori -induced gastritis was correlated with the upregulation of miR-146a and miR-155[13,14]. In addition, H. pylori infection could result in the downregulation of miRNAs.…”

Section: Introductionmentioning

confidence: 99%

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MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Feng¹,

Guo²,

Wang³

et al. 2019

WJG

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BACKGROUNDPediatric enteritis is one of the infectious diseases in the digestive system that causes a variety of digestive problems, including diarrhea, vomiting, and bellyache in children. Clinically, Helicobacter pylori (H. pylori) infection is one of the common factors to cause pediatric enteritis. It has been demonstrated that aberrant expression of microRNAs (miRNAs) is found in gastrointestinal diseases caused by H. pylori, and we discovered a significant increase of miR-32-5p in H. pylori-related pediatric enteritis. However, the exact role of miR-32-5p in it is still unknown.AIMTo investigate the role of aberrant miR-32-5p in pediatric enteritis induced by H. pylori.METHODSMiR-32-5p expression was detected by quantitative real time-polymerase chain reaction. The biological role of miR-32-5p in H. pylori-treated intestinal epithelial cells was evaluated by Cell Counting Kit-8 assay and flow cytometry. The potential target of miR-32-5p was predicted with TargetScanHuman and verified by luciferase assay. The downstream mechanism of miR-32-5p was explored by using molecular biology methods.RESULTSWe found that miR-32-5p was overexpressed in serum of H. pylori-induced pediatric enteritis. Further investigation revealed that H. pylori infection promoted the death of intestinal epithelial cells, and increased miR-32-5p expression. Moreover, miR-32-5p mimic further facilitated apoptosis and inflammatory cytokine secretion of intestinal epithelial cells. Further exploration revealed that SMAD family member 6 (SMAD6) was the direct target of miR-32-5p, and SMAD6 overexpression partially rescued cell damage induced by H. pylori. The following experiments showed that miR-32-5p/SMAD6 participated in the apoptosis of intestinal epithelial cells induced by transforming growth factor-β-activated kinase 1 (TAK1)-p38 activation under H. pylori infection.CONCLUSIONOur work uncovered the crucial role of aberrant expression of miR-32-5p in H. pylori–related pediatric enteritis, and suggested that the TAK1-p38 pathway is involved in it.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Feng¹,

Guo²,

Wang³

et al. 2019

WJG

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“…The relative expression levels of TLR9 mRNA were measured by real-time quantitative PCR based on the TaqMan ® System (Life Technologies, Carlsbad, CA, United States) within the StepOne Plus Real-Time PCR system 2.2.3 (Applied Biosystems) using a specific TaqMan probe for TLR9 (H00002973_m1) and two reference genes, GUSB (Hs00187320_m1) and TBP (Hs00187332_m1) which were tested in a previous study[19]. A pool of normal H. pylori- negative gastric tissue samples was used as a calibrator.…”

Section: Methodsmentioning

confidence: 99%

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

Susi¹,

Lourenço²,

Rasmussen³

et al. 2019

WJGO

Self Cite

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BACKGROUNDToll-like receptors (TLRs) are the first line of host defense, and are involved in Helicobacter pylori (H. pylori) recognition and activation of both inflammatory and carcinogenic processes. The 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 inconclusive.AIMTo evaluate whether TLR9 rs5743836 and rs187084 SNPs contribute to the risk of gastric carcinogenesis, and its influence on mRNA expression.METHODSA case-control study was conducted to evaluate two TLR9 SNPs (TLR9-1237 TC-rs5743836 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 polymorphism. All samples were tested for the H. pylori infection using Hpx1 and Hpx2 primers. Quantitative polymerase chain reaction by TaqMan® assay was used to quantify TLR9 mRNA from fresh gastric tissues (48 GC, 26 CG, and 14 C).RESULTSFor 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) groups. For 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 group. Moreover, 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 samples were grouped according to the polymorphic genotypes and the presence of H. pylori infection, an influence of TLR9-1237 TC + CC polymorphic genotypes (P = 0.0083) and H. pylori infection (P < 0.0001) was observed on the upregulation of mRNA expression.CONCLUSIONOur findings show that TLR9 rs5743836 and rs187084 polymorphisms are associated with a higher risk of carcinogenesis gastric, and that TLR9 mRNA levels can be modulated by TLR9-1237 TC + CC variant genotypes and H. pylori infection.

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“…O aumento da expressão do RNAm de TNF- em pacientes com neoplasia gástrica foi associado à presença do vírus H. pilory (Zabaglia et al, 2017;Hosseinzadeh et al, 2016 (Liu et al, 2008). Não houve diferença na expressão de RNAm de TNF-α em tecido neoplásico gástrico antes e após 3 semanas do emprego do quimioterápico cisplatina (Hosseinzadeh et al, 2016), assim como entre indivíduos que receberam ou não quimioterapia neoadjuvante para câncer gastroesofágico (Deans et al, 2006).…”

Section: Marcadores Inflamatóriosunclassified

“…Uma limitação do presente estudo se refere ao pequeno tamanho amostral, especialmente se comparado com estudos japoneses ou multicêntricos (Kim et al, 2017;Su et al, 2014;Liang et al, 2011). Entretanto, o número de casos avaliados foi igual ou superior (Augusto et al, 2007;Zabaglia et al, 2017) a outros estudos que analisaram a expressão do RNAm de citocinas inflamatórias. Na literatura, muitos estudos incluem pacientes com tumores variados do trato digestório (Matos-Neto et al, 2015;Shibata et al, 2008;Deans et al, 2006…”

Section: Forças E Limitações Do Estudounclassified

Marcadores inflamatórios em pacientes com neoplasia gástrica: níveis sanguíneos e expressão gênica

Ribeiro¹

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Expression of miRNA‐146a, miRNA‐155, IL‐2, and TNF‐α in inflammatory response to Helicobacter pylori infection associated with cancer progression

Cited by 20 publications

References 34 publications

MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

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

Marcadores inflamatórios em pacientes com neoplasia gástrica: níveis sanguíneos e expressão gênica

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