E-Selectin S128R Polymorphism is Associated with Cancer Risk: a Meta-analysis

Cheng, Da‐Chuan; Hao, Ying; Zhou, Wenling; Ma, Yanhong

doi:10.7314/apjcp.2014.15.7.3247

Cited by 3 publications

(4 citation statements)

References 34 publications

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“…Likewise, this allele was also linked to an elevated risk of relapse, metastasis and mortality among CRC patients [154][155][156]. A meta-analysis suggested rs5361 as an overall cancer risk factor among Caucasian and Asian ethnic groups [164]. In the same fashion as rs5361, rs5362 (A>G), rs5367 (A>G), and rs5368 (G>A) variant alleles were demonstrated to be associated with an increased risk of BC.…”

Section: E-selectinmentioning

confidence: 94%

Contribution of Endothelial Dysfunction to Cancer Susceptibility and Progression: A Comprehensive Narrative Review on the Genetic Risk Component

de Melo,

Tavares,

Pereira

et al. 2024

CIMB

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Venous thromboembolism (VTE) is a challenging clinical obstacle in oncological settings, marked by elevated incidence rates and resulting morbidity and mortality. In the context of cancer-associated thrombosis (CAT), endothelial dysfunction (ED) plays a crucial role in promoting a pro-thrombotic environment as endothelial cells lose their ability to regulate blood flow and coagulation. Moreover, emerging research suggests that this disorder may not only contribute to CAT but also impact tumorigenesis itself. Indeed, a dysfunctional endothelium may promote resistance to therapy and favour tumour progression and dissemination. While extensive research has elucidated the multifaceted mechanisms of ED pathogenesis, the genetic component remains a focal point of investigation. This comprehensive narrative review thus delves into the genetic landscape of ED and its potential ramifications on cancer progression. A thorough examination of genetic variants, specifically polymorphisms, within key genes involved in ED pathogenesis, namely eNOS, EDN1, ACE, AGT, F2, SELP, SELE, VWF, ICAM1, and VCAM1, was conducted. Overall, these polymorphisms seem to play a context-dependent role, exerting both oncogenic and tumour suppressor effects depending on the tumour and other environmental factors. In-depth studies are needed to uncover the mechanisms connecting these DNA variations to the pathogenesis of malignant diseases.

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Section: E-selectinmentioning

confidence: 94%

Contribution of Endothelial Dysfunction to Cancer Susceptibility and Progression: A Comprehensive Narrative Review on the Genetic Risk Component

de Melo,

Tavares,

Pereira

et al. 2024

CIMB

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show abstract

“…This suggests that it is a functional polymorphism. Furthermore, previous research has shown that SELE polymorphisms play a role in susceptibility to carcinoma development to some extent [6]. Endothelial cells express SELE, a key adhesion molecule known for its involvement in facilitating cell-cell contacts between cancer cells and endothelial monolayers during metastasis [7].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The relationship of E-selectin single-nucleotide polymorphisms with breast cancer in Iraqi Arab women

Zakariya

Almohaidi

Şimşek³

et al. 2022

Genomics Inform

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Breast cancer (BC) is a significant threat to female health, with both modifiable and non-modifiable risk factors. It is essential to monitor patients regularly and to raise population awareness. Increasing research also suggests that E-selectin (SELE) may increase tumor angiogenesis and the development of cancer. This study investigated SELE single-nucleotide polymorphisms (SNPs) in the following positions: rs5367T/C, rs5368C/T, rs5362T/G, and rs5362T/C. Using polymerase chain reaction, significant differences in allele and genotype frequencies were found between BC patients and controls. Position rs5368 was associated with an increased risk of BC for the CT and TT genotypes, with odds ratios (ORs) of 16.3 and 6.90 (Fisher probability=0.0001, p = 0.05). Women with the T allele had a 19.3-fold higher incidence of BC, while allele C may be a protective allele against BC (OR, 0.05). Heterozygous genotypes at rs5367, rs5362, and rs5362 were significantly more common in BC patients, with ORs of 5.70, 4.50, and 3.80, respectively. These SNPs may be associated with the risk of BC, because the frequency of mutant alleles was significantly higher in patients (OR: 4.26, 3.83, and 4.30, respectively) than in controls (OR: 0.23, 0.30, and 0.20, respectively). These SNPs may be considered a common genotype in the Iraqi population, with the wild-type allele having a protective fraction and the mutant allele having an environmental fraction. The results also revealed a 2-fold increase in gene expression in BC patients compared to controls, with a significant effect (p = 0.02). This study's findings confirm the importance of SELE polymorphisms in cancer risk prediction.

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“…The E-selectin S128R (A/C) polymorphism alters the binding specificity of the extracellular domain and thus facilitates ligand binding, which in turn improves the adhesion of lymphoid and myeloid cells to the endothelium [ 20 , 21 , 22 ]. In the E-selectin gene variants, the S128R polymorphism is of particular interest as it is clinically associated with increased cancer risk [ 23 ].…”

Section: Introductionmentioning

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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E-Selectin S128R Polymorphism is Associated with Cancer Risk: a Meta-analysis

Cited by 3 publications

References 34 publications

Contribution of Endothelial Dysfunction to Cancer Susceptibility and Progression: A Comprehensive Narrative Review on the Genetic Risk Component

Contribution of Endothelial Dysfunction to Cancer Susceptibility and Progression: A Comprehensive Narrative Review on the Genetic Risk Component

The relationship of E-selectin single-nucleotide polymorphisms with breast cancer in Iraqi Arab women

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

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