Polymorphisms of Receptor for Advanced Glycation end Products and Risk of Epithelial Ovarian Cancer in Chinese Patients

Zhang, Shuquan; Hou, Xuwei; Zi, Sihua; Wang, Yankui; Chen, Lijun; Kong, Beihua

doi:10.1159/000350073

Cited by 31 publications

(32 citation statements)

References 29 publications

(32 reference statements)

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“…Previous researches have reported that X-ray repair cross-complementing group 1 (XRCC1) is involved in the BER pathway through repairing DNA single-strand breaks, while both X-ray repair cross-complementing group 2 (XRCC2) and X-ray repair crosscomplementing group 3 (XRCC3) participate in the HRR pathway by repairing DNA doublestrand breaks [16][17][18][19]. As suggested by earlier studies, polymorphisms of these genes are related to thyroid cancer risk [6,[20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 89%

Association Studies Between XRCC1, XRCC2, XRCC3 Polymorphisms and Differentiated Thyroid Carcinoma

Yan¹,

Li²,

Li³

et al. 2016

Cell Physiol Biochem

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Background/Aims: DNA HRR pathway and BER pathway play vital roles in differentiated thyroid cancer (DTC) development, thus we supposed that polymorphisms of XRCC1, XRCC2, XRCC3 DNA repair genes are associated with thyroid cancer risk and progression. Methods: We searched the NCBI database for relevant literatures to determine eight SNPs to be included in our study (XRCC1: rs25487, rs25489, rs1799782; XRCC2: rs3218536; XRCC3: rs1799794, rs56377012, rs1799796, rs861539). Results: SNP of rs25487 was linked with a 53% decrease in DTC risk (OR: 0.47; 95%CI: 0.268-0.82; P = 0.01). For SNP of rs1799782, the homozygous TT genotype indicated a statistically significant 2-fold increased risk of DTC (OR: 2.09; 95%CI: 1.27-3.43; P < 0.001) after multivariate adjustment. For SNP of rs861539, the homozygous TT genotype suggested statistically significant 3-fold increased risk of DTC (OR: 3.02; 95%CI: 1.68-5.42; P < 0.001). No significant association between the other five SNPs and DTC risk. Besides that, female was linked with 47% increase in DTC risk (OR: 1.47; 95%CI: 1.062-2.04; P = 0.02) after multivariate adjustment. Similar results for most of the SNPs were obtained from subgroup analysis by different histological types of DTC. Haplotype analysis revealed that AGC and GGT haplotypes of XRCC1 polymorphisms were associated with DTC. Moreover, results from gene-gene interaction showed that XRCC1-rs25487, XRCC1- rs1799782 and XRCC3- rs861539 variants jointly contributed to a specifically increased risk of DTC, with the combination variant of rs1799782-CT heterozygote and rs861539-TT homozygote exhibiting a higher 3.66-fold risk of DTC (OR: 3.66; 95% CI: 1.476-9.091, P = 0.005). Conclusion: Polymorphisms of XRCC1 (rs25487, rs1799782) and XRCC3 (rs861539), may play a critical role in DTC development and progression. Furthermore, XRCC1 variant can interact with XRCC3 variant to significantly increase DTC susceptibility. Identifying these genetic risk markers could provide evidence for exploring the insight pathogenesis and develop novel therapeutic strategies for DTC.

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Section: Introductionmentioning

confidence: 89%

Association Studies Between XRCC1, XRCC2, XRCC3 Polymorphisms and Differentiated Thyroid Carcinoma

Yan¹,

Li²,

Li³

et al. 2016

Cell Physiol Biochem

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“…The expression of Gal-3 has been considered as a potential diagnostic and/or prognostic marker in stomach, colon-rectum, parathyroid, thyroid, breast, salivary glands, bladder, head and neck, prostate, and liver cancers [3,4,5,6,7,8]. Increasing evidence has revealed that Gal-3 protein plays an important role in pituitary tumorigenesis [9].…”

Section: Introductionmentioning

confidence: 99%

GAL3 Protein Expression is Related to Clinical Features of Prolactin-Secreting Pituitary Microadenoma and Predicts its Recurrence after Surgical Treatment

Dai

Li²,

Lu³

et al. 2014

Cell Physiol Biochem

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Background: Previous in vitro study showed that Galectin-3 (Gal-3) protein plays an important role in pituitary tumorigenesis, however, the association of Gal-3 expression with the clinical feature and prognosis of pituitary tumor in a clinical setting remains unknown. Methods: We enrolled 220 patients with prolactin-secreting pituitary adenomas (PA) who previously had transsphenoidal pituitary surgery. The Gal-3 expression was detected in the patients' PA samples using immunohistochemistry and those patients were followed up. A prolactin-secreting PA cell line, the MMQ cell line, was used to study the in vitro effect of Gal-3 on proliferation, migration and invasion of PA cells using small interfering RNA (siRNA) transfecton technique. The in vivo tumorgenesis in nude mice was also studied. Results: We found that Gal-3 expression was not related to age and sex, but positively associated with tumor invasion (P<0.001), tumor sizes (P<0.001) and pre-operative prolactin levels (P<0.001). The multivariate Cox analysis showed that the Gal-3 expression was closely associated with the recurrence of PA after the surgical treatment (HR =3.15, P=0.002). The in vitro studies showed that Gal-3 knock-down by the siRNA technique significantly inhibited the proliferation, migration and invasion ability of the MMQ cells, whereas Gal-3 siRNA transfection induced apoptosis of the MMQ cells. The in vivo tumorgenesis assay showed that Gal-3 siRNA transfection significantly inhibited the tumor volume in vivo compared to transfection of the control siRNA (P<0.001). Conclusion: Gal-3 regulates proliferation, apoptosis, migration and invasion of the MMQ cells. Gal-3 may be used as a tissue marker to evaluate the clinical feature and prognosis of PA patients.

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“…To date, numerous genetic variants have been identified in the RAGE gene, the majority of which are single-nucleotide polymorphisms (SNPs; Schmidt and Stern 2000). Ample studies have suggested that several RAGE gene polymorphisms, alone or in combination with other factors, are associated with the development or progression of various types of cancer, including gastric, lung, colorectal, breast, cervical, and ovarian cancer (Schenk et al 2001;Tesarova et al 2007;Gu et al 2008;Xu et al 2012;Zhang et al 2013;Qian et al 2014;). Such variations in genomic sequence have a potential to alter the function or expression of RAGE (Hudson et al 2001;Hofmann et al 2002), leading to changes in its final bioavailability and, thus, the carcinogenesis.…”

mentioning

confidence: 99%

RAGE Gene Polymorphism and Environmental Factor in the Risk of Oral Cancer

Chien

Lin

et al. 2015

J Dent Res

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Oral squamous cell carcinoma is a common neoplasm that is known to be causally associated with genetic factors and environmental carcinogens. The receptor for advanced glycosylation endproducts (RAGE) is a transmembrane protein of the immunoglobulin superfamily with broad specificity for multiple ligands, and it has been shown to play vital roles in several pathophysiologic processes, including diabetes, Alzheimer disease, renal disease, cardiovascular disease, and cancer. The present study aimed to assess the influences of RAGE gene polymorphisms, combined with environmental carcinogens on the predisposition to oral tumorigenesis. Five polymorphisms of the RAGE gene—including −374T>A (rs1800624), −429T>C (rs1800625), 1704G>T (rs184003), Gly82Ser (rs2070600), and a 63-bp deletion allele (−407 to −345)—were examined from 592 controls and 618 patients with oral cancer. We found that individuals carrying the polymorphic allele of rs1800625 are more susceptible to oral cancer (odds ratio [OR], 1.899; 95% confidence interval [CI], 1.355 to 2.661; adjusted OR [AOR], 2.053; 95% CI, 1.269 to 3.345) after adjustment for age, sex, betel nut chewing, and tobacco consumption. Moreover, we observed a significant association of rs1800625 variants with late-stage tumors (stage III/IV, OR, 1.736; 95% CI, 1.126 to 2.677; AOR, 1.771; 95% CI, 1.101 to 2.851) and large-size tumors (>2 cm in the greatest dimension; OR, 1.644; 95% CI, 1.083 to 2.493; AOR, 1.728; 95% CI, 1.089 to 2.741). Based on behavioral exposure of environmental carcinogens, the presence of 4 RAGE single-nucleotide polymorphisms (SNPs), combined with betel quid chewing and/or tobacco use, greatly augmented the risk of oral cancer. In addition, carriers of particular haplotypes of the 4 RAGE SNPs examined are more prone to develop oral cancer. These results indicate an involvement of RAGE SNP rs1800625 in the development of oral squamous cell carcinoma and implicate the interaction between RAGE gene polymorphisms and environmental mutagens as a predisposing factor of oral carcinogenesis.

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Polymorphisms of Receptor for Advanced Glycation end Products and Risk of Epithelial Ovarian Cancer in Chinese Patients

Cited by 31 publications

References 29 publications

Association Studies Between XRCC1, XRCC2, XRCC3 Polymorphisms and Differentiated Thyroid Carcinoma

Association Studies Between XRCC1, XRCC2, XRCC3 Polymorphisms and Differentiated Thyroid Carcinoma

GAL3 Protein Expression is Related to Clinical Features of Prolactin-Secreting Pituitary Microadenoma and Predicts its Recurrence after Surgical Treatment

RAGE Gene Polymorphism and Environmental Factor in the Risk of Oral Cancer

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