Polymorphisms of extrinsic death receptor apoptotic genes (FAS −670 G&gt;A, FASL −844 T&gt;C) in coronary artery disease

Kumar, G. Kishore; Kumar, G. Rajesh; Spurthi, Kondapalli Mrudula; Nivas, S.; Padala, Chiranjeevi; Ali, Altaf; Sahu, Sushanta Kumar; Nallari, Pratibha; Rani, H. Surekha

doi:10.1007/s10495-016-1232-7

Cited by 9 publications

(7 citation statements)

References 32 publications

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“…Linkage disequilibrium (LD) plots of controls and cases were generated using Haploview program [ 22 ]. Gene–gene interactions were determined by MDR analysis [ 23 ]. We have also compared the allele and genotype distribution for all clinical and histopathological characteristics of cases.…”

Section: Methodsmentioning

confidence: 99%

Synergistic effect of collagenase-1 (MMP1), stromelysin-1 (MMP3) and gelatinase-B (MMP9) gene polymorphisms in breast cancer

et al. 2017

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BackgroundExtracellular matrix degradation by matrix metalloproteinases (MMPs) is an important mechanism involved in tumor invasion and metastasis. Genetic variations of MMPs have shown association with multiple cancers. The present study is focused to elucidate the association of MMP-1, 3 and 9 genetic variants with respect to epidemiological and clinicopathological variables by haplotype, LD, MDR, survival in silico analyses among South Indian women.Material and methodsMMP3–1171 5A/6A and MMP9–1562 C/T SNPs were genotyped by Allele specific polymerase chain reaction and MMP1-1607 1G/2G polymorphism by restriction fragment length polymorphism assays respectively, in 300 BC patients and age-matched 300 healthy controls. Statistical analysis was performed using the SNPStats and SPSS software. Linkage disequilibrium and gene-gene interactions were performed using Haploview and MDR software respectively. Further, transcription factor binding sites in the promoter regions of SNPs under study were carried out using AliBaba2.1 software.ResultsWe have observed an increased frequency of 2G-allele of MMP1, 6A-allele of MMP3 and T-allele of MMP9 (p<0.05) respectively in BC subjects. The 2G-6A haplotype (minor alleles of MMP-1 and MMP-3 respectively) has shown an increased susceptibility to BC. Further, MMP polymorphisms were associated with the clinical characteristics of BC patients such as steroid hormone receptor status, lymph node involvement and metastasis. SNP combinations were in perfect LD in controls. MDR analysis revealed a positive interaction between the SNPs. 5-years survival rate and cox-regression analysis showed a significant association with clinicopathological variables.ConclusionOur results suggest that MMP1–1607 1G/2G, MMP3–1171 5A/6A and MMP9–1562 C/T gene polymorphisms have synergistic effect on breast cancer. The interactions of MMPs clinical risk factors such as lymph node involvement has shown a strong correlation and might influence the 5-years survival rate, suggesting their potential role in the breast carcinogenesis.

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Section: Methodsmentioning

confidence: 99%

Synergistic effect of collagenase-1 (MMP1), stromelysin-1 (MMP3) and gelatinase-B (MMP9) gene polymorphisms in breast cancer

et al. 2017

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“…Factor associated suicide (Fas) belongs to type I transmembrane glycoproteins with a molecular weight of 36 kDa, which can widely express a variety of virus-infected cells and tumor cells. Meanwhile, factor associated suicide ligand (FasL) is a type II transmembrane glycoprotein with a molecular weight of about 36-43 kDa, and is mainly expressed in activated T cells and NK cells [76]. As the interconnection between Fas and its ligand FasL, the cytotoxicity of tumor cells can be achieved through the pathway of Fas-FasL axis.…”

Section: Fasl Expressed On Nk Cells Exerts Anti-hepatocarcinoma Activmentioning

confidence: 99%

Recent Advances in Molecular Mechanisms of the NKG2D Pathway in Hepatocellular Carcinoma

Wang¹,

Li²,

Sun³

2020

Biomolecules

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Hepatocellular carcinoma is a common malignant tumor with high mortality. Its malignant proliferation, invasion, and metastasis are closely related to the cellular immune function of the patients. NKG2D is a key activated and type II membrane protein molecule expressed on the surface of almost all NK cells. The human NKG2D gene is 270 kb long, located at 12p12.3–p13.1, and contains 10 exons and 9 introns. The three-dimensional structure of the NKG2D monomeric protein contains two alpha-helices, two beta-lamellae, and four disulfide bonds, and its’ signal of activation is transmitted mainly by the adaptor protein (DAP). NKG2D ligands, including MICA, MICB, and ULBPs, can be widely expressed in hepatoma cells. After a combination of NKG2D and DAP10 in the form of homologous two polymers, the YxxM motif in the cytoplasm is phosphorylated and then signaling pathways are also gradually activated, such as PI3K, PLCγ2, JNK-cJunN, and others. Activated NK cells can enhance the sensitivity to hepatoma cells and specifically dissolve by releasing a variety of cytokines (TNF-α and IFN-γ), perforin, and high expression of FasL, CD16, and TRAIL. NK cells may specifically bind to the over-expressed MICA, MICB, and ULBPs of hepatocellular carcinoma cells through the surface activating receptor NKG2D, which can help to accurately identify hepatoma, play a critical role in anti-hepatoma via the pathway of cytotoxic effects, and obviously delay the poor progress of hepatocellular carcinoma.

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“…CAD develops as a result of vascular tract stenosis or occlusion caused by coronary atherosclerotic lesions and several environmental and lifestyle factors (Campbell et al, 1998;Erbel and Görge, 2014;Bullock-Palmer, 2015). Previous experimental studies at the molecular level have indicated that many genetic factors, including the genes encoding angiotensinogen and angiotensin-converting enzyme, hepatic lipase, insulin receptor substrate-1, kinesin family member 6, cholesteryl ester transfer protein, ATP-binding cassette subfamily A member 1, and apoptotic extrinsic death receptor, have an important role in the risk of CAD development (Bonfim-Silva et al, 2016;Cyrus et al, 2016;Kishore Kumar et al, 2016;Mohammadzadeh et al, 2016;Vatte et al, 2016;Zhang et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Effect of polymorphisms in interleukin-18 gene on the susceptibility to coronary artery disease in a Chinese population

Chen²,

Gao

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Coronary artery disease (CAD) has a high mortality rate in several countries. Interleukin (IL)-18 has been previously correlated with atherosclerotic plaque rupture. In this case-control study, the relationship between -607A/C and -372C/G promoter polymorphisms in IL-18 and risk of CAD development was investigated. A total of 326 CAD patients were consecutively recruited from the First Hospital of Yulin between March 2013 and May 2015. The IL-18 -607A/C and -372C/G polymorphisms were genotyped by polymerase chain reactionrestriction fragment length polymorphism. Patients with CAD had a higher body mass index, a history of hypertension or diabetes (all P < 0.001), cigarette smoking habit (P = 0.002); as well as higher plasma total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels (all P < 0.001) and lower high-density lipoprotein cholesterol (P < 0.001) levels compared to the control subjects. Unconditional logistic regression analysis revealed significant correlation between the CC genotype of IL-18 -607A/C and CAD development, compared to the AA genotype [adjusted odds ratio (OR) = 2.42; 95% confidence interval (CI) = 1.52-3.89; P < 0.001]. The recessive model showed a significant association between the CC genotype of IL-18 -607A/C and an increased risk of CAD, compared to the AA+AC genotype (OR = 2.51, 95%CI = 1.65-3.85). However, IL-18 -372C/G did not contribute to the risk of glioma development in the co-dominant, dominant, and recessive models. Therefore, the IL-18 -607C/A polymorphism was significantly correlated with the risk of CAD development.

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Polymorphisms of extrinsic death receptor apoptotic genes (FAS −670 G>A, FASL −844 T>C) in coronary artery disease

Cited by 9 publications

References 32 publications

Synergistic effect of collagenase-1 (MMP1), stromelysin-1 (MMP3) and gelatinase-B (MMP9) gene polymorphisms in breast cancer

Synergistic effect of collagenase-1 (MMP1), stromelysin-1 (MMP3) and gelatinase-B (MMP9) gene polymorphisms in breast cancer

Recent Advances in Molecular Mechanisms of the NKG2D Pathway in Hepatocellular Carcinoma

Effect of polymorphisms in interleukin-18 gene on the susceptibility to coronary artery disease in a Chinese population

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