E-Selectin S128R Gene Polymorphism in Gastric Cancer

Liarmakopoulos, Emmanouil; Gazouli, Maria; Aravantinos, G.; Theodoropoulos, George; Rizos, Spyros; Vaiopoulou, Anna; Kouraklis, Gregory; Nikiteas, Nikolaos

doi:10.5301/jbm.2012.9582

Cited by 8 publications

(8 citation statements)

References 26 publications

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“…S128R E-selectin has been shown to bind nonfucosylated K562 cells and is able to bind neuraminidase treated HL-60 cells, both of which cannot bind to wild-type E-selectin, clearly demonstrating that this naturally occurring E-selectin mutant can bind ligands other than sLe x (Revelle et al 1996;Rao et al 2002). If selectin/sLe x were required for leukocyte trafficking, it would be expected that persons carrying this mutation would be protected from inflammation; in contrast however, the S128R mutation is associated with increased risk for coronary artery disease (Wenzel et al 1996;Ghilardi et al 2004), cancer (Nadi et al 2007;Khazen et al 2009;Liarmakopoulos et al 2012), and importantly with increases in leukocyte trafficking (Khazen et al 2009;Liarmakopoulos et al 2012). To date, several mouse models that have reduced ability to express sLe x structures or deletion of endothelial selectins have been produced.…”

Section: Dw Scott and Rp Patelmentioning

confidence: 99%

Endothelial heterogeneity and adhesion molecules N-glycosylation: Implications in leukocyte trafficking in inflammation

Scott

Patel

2013

Glycobiology

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Inflammation is a major contributing element to a host of diseases with the interaction between leukocytes and the endothelium being key in this process. Much is understood about the nature of the adhesion molecule proteins expressed on any given leukocyte and endothelial cell that modulates adhesive interactions. Although it is appreciated that these proteins are heavily glycosylated, relatively little is known about the roles of these posttranslational modifications and whether they are regulated, and if so how during inflammation. Herein, we suggest that a paucity in this understanding is one major reason for the lack of successful therapies to date for modulating leukocyte-endothelial interactions in human inflammatory disease and discuss developing paradigms of (i) how endothelial adhesion molecule glycosylation (with a focus on N-glycosylation) maybe a critical element in understanding endothelial heterogeneity between different vascular beds and species, (ii) how adhesion molecule N-glycosylation may be under distinct, and as yet, unknown modes of regulation during inflammatory stress to affect the inflammatory response in a vascular bed- and disease-specific manner (analogous to a "zip code" for inflammation) and finally (iii) to underscore the concept that a fuller appreciation of the role of adhesion molecule glycoforms is needed to provide foundations for disease and tissue-specific targeting of inflammation.

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Section: Dw Scott and Rp Patelmentioning

confidence: 99%

Endothelial heterogeneity and adhesion molecules N-glycosylation: Implications in leukocyte trafficking in inflammation

Scott

Patel

2013

Glycobiology

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“…The S128R polymorphism (A>C variation), the most common SNP of the E-selectin gene, facilitates ligand binding, which in turn increases the adhesion of lymphoid and myeloid cells to the endothelium. The E-selectin S128R polymorphism is associated with an increased risk of several cancers including gastric [ 25 , 26 ], colorectal [ 27 ] and pancreatic [ 28 ] cancers. However, a very limited number of studies investigating the association of the E-selectin S128R polymorphism with breast cancer susceptibility have revealed contradictory results.…”

Section: Discussionmentioning

confidence: 99%

Association of E-selectin S128R polymorphism with hereditary breast carcinoma susceptibility in Turkish patients without BRCA1/2 germline mutations

Yararbaş

Atalay

2018

Balkan Journal of Medical Genetics

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Inherited genetic factors play an important role in breast cancer susceptibility. The BRCA1 and BRCA2 mutations are the most well-known genetic factors associated with increased risk of breast cancer. E-selectin is a cell surface glycoprotein and its serum levels are known to increase in various cancers. The present retrospective study aimed to evaluate whether E-selectin S128R polymorphism (NG_012124.1: g.7161A>C, NM_000450.2: c.445A>C, NP_000441.2: p.Ser149Arg), which is known to have a role in cancer risk, is associated with breast cancer susceptibility in BRCA 1/2 mutation non carriers with breast cancer. The study included 90 patients with breast cancer and 270 healthy controls. All breast cancer patients were screened for BRCA 1/2 mutations and confirmed to be BRCA 1/2 mutation non carriers before inclusion in the study. Genotyping for the E-selectin S128R polymorphism was performed using real-time polymerase chain reaction (PCR) analysis. The frequencies of the AA, AC and CC genotypes were 70.0, 25.5 and 4.5%, respectively, in the patient group and 79.25, 19.25 and 1.5%, respectively, in the controls. The frequencies of A and C alleles were 84.8 and 15.2% in the patient group, respectively, and 88.9 and 11.1%, respectively, in the controls. No significant differences were determined in the genotype and allele frequencies of the E-selectin S128R polymorphism between the patient and control groups (p = 0.095). The S128R (A/C) polymorphism was not found to be associated with an increased risk of breast cancer [odds ratio (OR) = 0.69; 95% confidence interval (95% CI): 0.43-1.10; p = 0.1248). There was no association between the S128R polymorphism and breast cancer susceptibility in BRCA 1/2 mutation non carriers with breast cancer in the studied Turkish population. Further studies with larger sample sizes are needed to validate our findings.

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“…However, more experiments are required to verify the above. E-selectin, the protein encoded by the SELE gene, mediates the progression and invasion of GC through different mechanisms, including promoting angiogenesis by activating the Src-PI3K pathway [150,151]. A positive correlation has been observed in GC between the serum expression levels of circulating E-selectin and tumor progression and metastasis, leading to a poor prognosis [152][153][154][155].…”

Section: A a B Bmentioning

confidence: 99%

“…A positive correlation has been observed in GC between the serum expression levels of circulating E-selectin and tumor progression and metastasis, leading to a poor prognosis [152][153][154][155]. Liarmakopoulos et al [150] demonstrated that the E-selectin S128R C allele was related to dismal survival in GC patients.…”

Section: A a B Bmentioning

confidence: 99%

Prognostic biomarkers and molecular pathways mediating Helicobacter pylori–induced gastric cancer: a network-biology approach

2023

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Cancer of the stomach is the second most frequent cancer-related death worldwide. The survival rate of patients with gastric cancer (GC) remains fragile. There is a requirement to discover biomarkers for prognosis approaches. Helicobacter pylori in the stomach is closely associated with the progression of GC. We identified the genes associated with poor/favorable prognosis in H. pylori–induced GC. Multivariate statistical analysis was applied on the Gene Expression Omnibus (GEO) dataset GSE54397 to identify differentially expressed miRNAs (DEMs) in gastric tissues with H. pylori–induced cancer compared with the H. pylori–positive with non-cancerous tissue. A protein interaction map (PIM) was built and subjected to DEMs targets. The enriched pathways and biological processes within the PIM were identified based on substantial clusters. Thereafter, the most critical genes in the PIM were illustrated, and their prognostic impact in GC was investigated. Considering p-value less than 0.01 and |Log2 fold change| as >1, five microRNAs demonstrated significant changes among the two groups. Gene functional analysis revealed that the ubiquitination system, neddylation pathway, and ciliary process are primarily involved in H. pylori–induced GC. Survival analysis illustrated that the overexpression of DOCK4, GNAS, CTGF, TGF-b1, ESR1, SELE, TIMP3, SMARCE1, and TXNIP was associated with poor prognosis, while increased MRPS5 expression was related to a favorable prognosis in GC patients. DOCK4, GNAS, CTGF, TGF-b1, ESR1, SELE, TIMP3, SMARCE1, TXNIP, and MRPS5 may be considered prognostic biomarkers for H. pylori–induced GC. However, experimental validation is necessary in the future.

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E-Selectin S128R Gene Polymorphism in Gastric Cancer

Abstract: The E-selectin S128R C allele may confer an increased susceptibility to gastric cancer development and correlate with a poor prognosis.

Cited by 8 publications

References 26 publications

Endothelial heterogeneity and adhesion molecules N-glycosylation: Implications in leukocyte trafficking in inflammation

Endothelial heterogeneity and adhesion molecules N-glycosylation: Implications in leukocyte trafficking in inflammation

Association of E-selectin S128R polymorphism with hereditary breast carcinoma susceptibility in Turkish patients without BRCA1/2 germline mutations

Prognostic biomarkers and molecular pathways mediating Helicobacter pylori–induced gastric cancer: a network-biology approach

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