EGFR and Bcl-2 in gastric mucosa of children infected with Helicobacter pylori

Ryszczuk, Ewa; Roszko-Kirpsza, Izabela; Guzińska‐Ustymowicz, Katarzyna; Olejnik, Beata Janina; Kaczmarski, Maciej; Maciorkowska, Elżbieta

doi:10.5604/17322693.1198272

Cited by 3 publications

(4 citation statements)

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“…These results are in agreement with other studies showing that Bcl-2 not only inhibits apoptosis, but also suppresses cellular proliferative activity (Bélanger et al, 2005). According to Ryszczuk et al (2016) Bcl-2 is over expressed in antral gastritis of H. pylori infected children, in both surface epithelial and gland cells. COX-2 (Cyclooxygenase 2) is an enzyme which catalyzes prostaglandin synthesis (Vane et al, 1998).…”

Section: Transporters and Enzymessupporting

confidence: 92%

“…Therefore, anti-EGFR agents have been evaluated for treatment of advanced GC, with variable results between studies, and no overall benefit according to a recent meta-analysis (Kim et al, 2017). In infected children, EGFR is overexpressed mainly in epithelial gastric cells (Maciorkowska et al, 2009;Ryszczuk et al, 2016). CRABP1 (Cellular retinoic acid-binding protein 1) is responsible for binding retinoic acid transporting it into cells.…”

Section: Receptorsmentioning

confidence: 99%

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Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

et al. 2020

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Helicobacter pylori (H. pylori) is well-known to be involved in gastric carcinogenesis, associated with deregulation of cell proliferation and epigenetic changes in cancerrelated genes. H. pylori infection is largely acquired during childhood, persisting long-term in about half of infected individuals, a subset of whom will go on to develop peptic ulcer disease and eventually gastric cancer, however, the sequence of events leading to disease is not completely understood. Knowledge on carcinogenesis and gastric damage-related biomarkers is abundant in adult populations, but scarce in children. We performed an extensive literature review focusing on gastric cancer related biomarkers identified in adult populations, which have been detected in children infected with H. pylori. Biomarkers were related to expression levels (RNA or protein) and/or methylation levels (DNA) in gastric tissue or blood of infected children as compared to non-infected controls. In this review, we identified 37 biomarkers of which 24 are over expressed, three are under expressed, and ten genes are significantly hypermethylated in H. pylori-infected children compared to healthy controls in at least 1 study. Only four of these biomarkers (pepsinogen I, pepsinogen II, gastrin, and SLC5A8) have been studied in asymptomatically infected children. Importantly, 13 of these biomarkers (β-catenin, C-MYC, GATA-4, DAPK1, CXCL13, DC-SIGN, TIMP3, EGFR, GRIN2B, PIM2, SLC5A8, CDH1, and VCAM-1.) are consistently deregulated in infected children and in adults with gastric cancer. Future studies should be designed to determine the clinical significance of these changes in infection-associated biomarkers in children and their persistence over time. The effect of eradication therapy over these biomarkers in children if proven significant, could lead to modifications in treatment guidelines for younger populations, and eventually promote the development of preventive strategies, such as vaccination, in the near future.

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Section: Transporters and Enzymessupporting

confidence: 92%

Section: Receptorsmentioning

confidence: 99%

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

et al. 2020

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“…Currently, it is known that genomes of Helicobacter pylori contain genes, including vacA, iceA, cagA and abA, associated with an increased pathogenicity of the microorganism. The most virulent Cag positive (+) strains of Helicobacter pylori are thought to cause an intense cellular response: inflammation of the gastric and duodenal mucosa, cell proliferation and cell death (4)(5)(6) . Chronic gastritis and gastroduodenitis is a clinical and morphological diagnosis; therefore, the diagnostic "gold standard" should be a morphological examination of the mucous membrane of the stomach, which makes it possible to determine the depth and nature of the lesion (7) .…”

Section: Introductionmentioning

confidence: 99%

Morphological changes of the mucous membrane in children with chronic gastroduodenal pathology and infection with cytotoxic strains of Helicobacter pylori

Руденко¹,

Khromykh²,

Shalamai³

et al. 2018

PEDIATR MED RODZ

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Helicobacter pylori plays the main role in the development of chronic pathology of the gastroduodenal area. Helicobacter pylori infects 25% of the population in developed countries and up to 90% in developing countries. The most virulent are CagA positive (+) strains of Helicobacter pylori, which cause an intense cellular response, i.e. inflammation of the stomach mucous membrane, cell proliferation and cell death. Material and methods: We examined 75 children, aged 10 to 18 years, with chronic gastroduodenal pathology associated with Helicobacter pylori. A morphological and morphometric study of the stomach mucous membrane was performed depending on the presence of cytotoxic strains of Helicobacter pylori. Results: In children infected with CagA (+) strains of Helicobacter pylori, active and deep chronic gastritis and gastroduodenitis [21 (28.00%), 20 (26.67%), respectively] were more common than in children with CagA (−) strains [10 (13.33%), 13 (17.33%), respectively]. Discussion: Morphological studies provide an opportunity to determine quantitative and qualitative changes in the mucous membrane of the stomach in gastroduodenal pathology associated with Helicobacter infection. This increases the quality of diagnosis and predicts the course of the disease. Conclusion:A morphological study has shown that the presence of cytotoxic strains of Helicobacter pylori contributes to more significant changes in the gastric mucosa in children with chronic gastroduodenal pathology.

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“…The increased levels of p38MAPK (38-kD tyrosine phosphorylated protein kinase) will result in the upregulation of H. pylori proliferation [ 24 ]. Increased expression of anti-apoptotic gene Bcl-2 has also been found in the gastric mucosa infected by H. pylori in children [ 25 ]. The upregulation of H. pylori infection on the pro-apoptotic gene, BCL-2-associated protein X (BAX), is higher than its induction of B cell lymphoma gene 2 (BCL-2), which will result in the apoptosis in patients with chronic gastritis [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Quercetin from Polygonum capitatum Protects against Gastric Inflammation and Apoptosis Associated with Helicobacter pylori Infection by Affecting the Levels of p38MAPK, BCL-2 and BAX

et al. 2017

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Helicobacter pylori-associated gastritis is a major threat to public health and Polygonum capitatum (PC) may have beneficial effects on the disease. However, the molecular mechanism remains unknown. Quercetin was isolated from PC and found to be a main bioactive compound. The effects of quercetin on human gastric cancer cells GES-1 were determined by xCELLigence. H. pylori-infected mouse models were established. All mice were divided into three groups: control (CG, healthy mice), model (MG, H. pylori infection) and quercetin (QG, mouse model treated by quercetin) groups. IL-8 (interleukin-8) levels were detected via enzyme-linked immunosorbent assay (ELISA). Cell cycle and apoptosis were measured by flow cytometry (FCM). Quantitative reverse transcription PCR (qRT-PCR) and Western Blot were used to detect the levels of p38MAPK (38-kD tyrosine phosphorylated protein kinase), apoptosis regulator BCL-2-associated protein X (BAX) and B cell lymphoma gene 2 (BCL-2). The levels of IL-8 were increased by 8.1-fold in a MG group and 4.3-fold in a QG group when compared with a CG group. In a MG group, G0–G1(phases of the cell cycle)% ratio was higher than a CG group while S phase fraction was lower in a model group than in a control group (p < 0.01). After quercetin treatment, G0–G1% ratio was lower in a QG group than a MG group while S phase fraction was higher than a MG group (p < 0.01). Quercetin treatment reduced the levels of p38MAPK and BAX, and increased the levels of BCL-2 when compared with a MG group (p < 0.05). Quercetin regulates the balance of gastric cell proliferation and apoptosis to protect against gastritis. Quercetin protects against gastric inflammation and apoptosis associated with H. pylori infection by affecting the levels of p38MAPK, BCL-2 and BAX.

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EGFR and Bcl-2 in gastric mucosa of children infected with Helicobacter pylori

Abstract: Increased expression of EGFR and Bcl-2 proteins in the epithelial cells and a statistically significant positive correlation between the numbers of cells expressing EGFR and Bcl-2 in H. pylori infected children could suggest increased regeneration abilities of gastric mucosa.

Cited by 3 publications

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Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

Morphological changes of the mucous membrane in children with chronic gastroduodenal pathology and infection with cytotoxic strains of Helicobacter pylori

Quercetin from Polygonum capitatum Protects against Gastric Inflammation and Apoptosis Associated with Helicobacter pylori Infection by Affecting the Levels of p38MAPK, BCL-2 and BAX

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