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Significant association between IL-18 and OCT4 gene polymorphisms in susceptibility and clinical characteristics of prostate cancer 被引量:2

Significant association between IL-18 and OCT4 gene polymorphisms in susceptibility and clinical characteristics of prostate cancer
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摘要 Objective Recent studies have shown abnormal expression of octamer-binding transcription factor 4(OCT4) and interleukin-18(IL-18) to be related to cancer. However, the molecular mechanisms by which the IL-18 and OCT4 gene polymorphisms are associated with prostate cancer remain unclear. In this study, we aimed to determine whether the presence of IL-18 and OCT4 polymorphisms were associated with size, grade, tumor, nodes and metastasis(TNM) stage, or survival in patients with prostate cancer.Methods Polymorphisms in OCT4 and IL-18 genes were evaluated to determine susceptibility to prostate cancer in 120 patients. A control group consisted of 125 Chinese participants. Genotyping was performed using TaqMan allelic discrimination assays, and statistical analysis was performed using SPSS. Results No association was found between OCT4 and IL-18 gene polymorphisms and prostate cancer susceptibility. For OCT4 AA and IL-18-607 CC genotypes, there was a significant association with higher tumor grade(P = 0.03 and P = 0.025) and stage(P = 0.04 and P = 0.001). The OCT4 and IL-18-137 GG genotype was correlated with higher tumor grade(P = 0.028) and stage(P = 0.008). Furthermore, OCT4 AA was significantly more frequent in patients with lymph node metastasis(P = 0.02) and distant metastasis(P = 0.01). The Cox proportional hazard model showed that tumor grade and stage grouping were independent prognostic factors but IL-18 and OCT4 polymorphisms were not. Conclusion The OCT4 gene may have a profound effect on prostate cancer risk. Polymorphism variants in the IL-18(IL-18-607 and IL-18-137) and OCT4 genes may be associated with poor prognoses for individuals with prostate cancer. Objective Recent studies have shown abnormal expression of octamer-binding transcription factor 4(OCT4) and interleukin-18(IL-18) to be related to cancer. However, the molecular mechanisms by which the IL-18 and OCT4 gene polymorphisms are associated with prostate cancer remain unclear. In this study, we aimed to determine whether the presence of IL-18 and OCT4 polymorphisms were associated with size, grade, tumor, nodes and metastasis(TNM) stage, or survival in patients with prostate cancer.Methods Polymorphisms in OCT4 and IL-18 genes were evaluated to determine susceptibility to prostate cancer in 120 patients. A control group consisted of 125 Chinese participants. Genotyping was performed using TaqMan allelic discrimination assays, and statistical analysis was performed using SPSS. Results No association was found between OCT4 and IL-18 gene polymorphisms and prostate cancer susceptibility. For OCT4 AA and IL-18-607 CC genotypes, there was a significant association with higher tumor grade(P = 0.03 and P = 0.025) and stage(P = 0.04 and P = 0.001). The OCT4 and IL-18-137 GG genotype was correlated with higher tumor grade(P = 0.028) and stage(P = 0.008). Furthermore, OCT4 AA was significantly more frequent in patients with lymph node metastasis(P = 0.02) and distant metastasis(P = 0.01). The Cox proportional hazard model showed that tumor grade and stage grouping were independent prognostic factors but IL-18 and OCT4 polymorphisms were not. Conclusion The OCT4 gene may have a profound effect on prostate cancer risk. Polymorphism variants in the IL-18(IL-18-607 and IL-18-137) and OCT4 genes may be associated with poor prognoses for individuals with prostate cancer.
出处 《Oncology and Translational Medicine》 2019年第3期123-130,共8页 肿瘤学与转化医学(英文版)
基金 Supported by grants from the China Postdoctoral Science Foundation(No.2014M139951) the Science and Technology Project of Nantong,Jiangsu Province(No.MS22016043)
关键词 clinical characteristics interleukin-18(IL-18) octamer-binding TRANSCRIPTION factor 4(OCT4) polymorphism prostate cancer clinical characteristics interleukin-18(IL-18) octamer-binding transcription factor 4(OCT4) polymorphism prostate cancer
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  • 1Okamura H, Tsutsui H, Komatsu T, et al. Cloning of a new cytokine that induces IFN-γ production by T cells. Nature. 1995. 378: 88-91.
  • 2Oshikawa K, Shi F, Rakhmilevich AL, et al. Synergistic inhibition of tumor growth in a murine mammary adenocarcinoma model by combinational gene therapy using IL-12, pro-IL-18, and IL-lbeta convening enzyme cDNA. Proc Natl Acad Sci USA, 1999, 96: 13351-13356
  • 3Oshikawa K, Shi F, Rakhmilevich AL, et al. Interleukin-18 acts as an angiogenesis and tumor suppressor. FASEB J, 1999,13: 2195-2202.
  • 4Vidal-Vanaclocha F, Fantuzzi G, Mendoza L, et al. IL-18 regulates 1L-1beta-dependent hepatic melanoma metastasis via vascular cell adhesion molecule-1. Proc Natl Acad Sci USA, 2000, 97: 734-739.
  • 5Mendoza L, Carrascal T, De Luca AM, et al. Hydrogen peroxide mediates vascular cell adhesion molecule-1 expression from interleukin-18-activated hepatic sinusoidal endothelium: implications for circulating cancer cell arrest in the murine liver. Hepatology, 2001, 34:298-310
  • 6Morel JC, Park CC, Woods JM, et al.A novel--role for interleukin-18 in adhesion molecule induction through NF kappa B and phosphatidylinositol(PI) 3-kinase-dependent signal transduction pathways. J Biol Chem,2001, 276:37069-37075.
  • 7Merendino RA, Gangemi S, Ruello A, et al. Serum levels of interleukin-18 and sICAM-1 in patients affected by breast cancer:preliminary considerations. Int J Biol Markers, 2001, 16: 126-129.
  • 8Berx G, Cleton-Jansen AM, Strumane K, et al. E-cadherin inactivated in a majority of invasive human lobular breast cancers by truncation mutations throughout its extracellular domain. Oncogene , 1996, 13:1919-1925.
  • 9Berx G, Cleton-Jansen AM, Nollet F, et al. E-cadherin is a tumor/invasion suppressor gene mutated in human lobular breast cancers.EMBO J, 1995, 14: 6107-6115.
  • 10Melki JR, Vincent PC, Brown RD, et al. Hypermethylation of E-cadherin in leukemia. Blood, 2000, 95:3208-3213.

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