Cellular and molecular aspects of gastric cancer

Smith, M. G.; Hold, Georgina L.; Tahara, Eiichi; El-Omar, Emad

doi:10.3748/wjg.v12.i19.2979

Cited by 204 publications

(185 citation statements)

References 139 publications

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“…Gastric cancer cells express a variety of factors, such as growth factors and cytokines, through interaction with microenvironment (Smith et al, 2006). Interactions between tumor and stromal cells have been reported to create a unique microenvironment that is essential for tumor growth and metastasis (Whiteside, 2008).…”

Section: Introductionmentioning

confidence: 99%

S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

Kwon

Moon

Park

et al. 2013

Molecules and Cells

107

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S100A8 and S100A9 (S100A8/A9) are low-molecular weight members of the S100 family of calcium-binding proteins. Recent studies have reported S100A8/A9 promote tumorigenesis. We have previously reported that S100A8/A9 is mostly expressed in stromal cells and inflammatory cells between gastric tumor cells. However, the role of environmental S100A8/A9 in gastric cancer has not been defined. We observed in the present study the effect of S100A8/A9 on migration and invasion of gastric cancer cells. S100A8/ A9 treatment increased migration and invasionat lower concentrations that did not affect cell proliferation and cell viability. S100A8/A9 caused activation of p38 mitogenactivated protein kinase (MAPK) and nuclear factor-κB (NF-κB). The phosphorylation of p38 MAPK was not affected by the NF-κB inhibitor Bay whereas activation of NF-κB was blocked by p38 MAPK inhibitor SB203580, indicating that S100A8/A9-induced NF-κB activation is mediated by phosphorylation of p38 MAPK. S100A8/A9-induced cell migration and invasion was inhibited by SB203580 and Bay, suggesting that activation of p38 MAPK and NF-κB is involved in the S100A8/A9 induced cell migration and invasion. S100A8/A9 caused an increase in matrix metalloproteinase 2 (MMP2) and MMP12 expression, which were inhibited by SB203580 and Bay. S100A8/A9-induced cell migration and invasion was inhibited by MMP2 siRNA and MMP12 siRNA, indicating that MMP2 and MMP12 is related to the S100A8/A9 induced cell migration and invasion. Taken together, these results suggest that S100A8/A9 promotes cell migration and invasion through p38 MAPKdependent NF-κB activation leading to an increase of MMP2 and MMP12 in gastric cancer.

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Section: Introductionmentioning

confidence: 99%

S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

Kwon

Moon

Park

et al. 2013

Molecules and Cells

107

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“…In Iranian population, GC is the first cause of cancer deaths in both sexes (Smith et al, 2006;Malekzadeh et al 2009). The etiology of GC is not clearly known.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Insulin Like Growth Facror-1 Genetic Polymorphism with Gastric Cancer Susceptibility and Clinicopathological Features

Farahani

Azimzadeh²,

Rostami³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Gastric cancer (GC) is one of the most common malignancies in the world. It is the first cause of cancer deaths in both sexes In Iranian population. Circulating insulin-like growth factor-one (IGF-1) levels have been associated for gastric cancer. IGF-1 protein has central roles involved in the regulation of epithelial cell growth, proliferation, transformation, apoptosis and metastasis. Single nucleotide polymorphism in IGF-1 regulatory elements may lead to alter in IGF-1expression level and GC susceptibility. The aim of this study was to investigate the influence of IGF-1 gene polymorphism (rs5742612) on risk of GC and clinicopathological features for the first time in Iranian population. In total, 241 subjects including 100 patients with GC and 141 healthy controls were recruited in our study. Genotypes were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay with DNA from peripheral blood. The polymorphism was statistically analyzed to investigate the relationship with the risk of GC and clinicopathological properties. Logistic regression analysis revealed that there was no significant association between rs5742612 and the risk of GC. In addition, no significant association between genotypes and clinicopathological features was observed (p value>0.05). The frequencies of the CC, CT, and TT genotypes were 97%, 3%, and 0%, respectively, among the cases, and 97.9%, 2.1%, and 0%, respectively, among the controls. CC genotype was more frequent in cases and controls. The frequencies of C and T alleles were 98.9% and 1.1% in controls and 98.5% and 1.5% in patient respectively. Our results provide the first evidence that this variant is rare in Iranian population and it may not be a powerful genetic predisposing biomarker for prediction GC clinicopathological features in an Iranian population.

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“…Therefore, we have examined the interaction between NAT2 phenotype and H pylori [22] . NH3 increases the incidence and size of g astric adenocarcinomas in rats pretreated with N-methyl-N' -nitro-N-nitrosoguanidine [23,24] . Moreover, H pylori infection plays a role in the pathogenesis of active chronic gastritis by generating toxic monochloramine (NH2Cl) from an oxidant (HOCl) that is a product of activated neutrophils and NH3 [25] .…”

Section: Discussionmentioning

confidence: 99%

NAT2polymorphism in Omani gastric cancer patients-risk predisposition and clinicopathological associations

Al-Moundhri

Al-Kindi

Al-Nabhani

et al. 2007

WJG

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AIM:To study whether N-acetyltransferase 2 (NAT2 ) genotypes and phenotypes are associated with increased risk factor for gastric cancer in Omani patients and to study the clinico-pathological correlations and the prognostic significance of NAT2 . control subjects. NAT2 genotyping was performed using DNA sequencing. The prognostic significance of NAT2 and other clinicopathological features was assessed by univariate and multivariate analyses. M E T H O D S : RESULTS:We observed no significant association between NAT2 genotypes and phenotypes and gastric cancer risk. The NAT2 phenotype polymorphisms and gastric cancer risk predisposition were not modified by concomitant H pylori infection and smoking. There was no significant association between NAT2 and clinicopathological features, and NAT2 had no independent prognostic significance. CONCLUSION:In the current study, NAT2 genotypes and phenotypes are not associated with gastric cancer risk predisposition. Moreover NAT2 phenotypes had no clinicopathological associations or prognostic significance.

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Cellular and molecular aspects of gastric cancer

Cited by 204 publications

References 139 publications

S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

Evaluation of Insulin Like Growth Facror-1 Genetic Polymorphism with Gastric Cancer Susceptibility and Clinicopathological Features

NAT2polymorphism in Omani gastric cancer patients-risk predisposition and clinicopathological associations

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