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Sun G.,Nantong University | Shi L.,Jiangsu University | Yan S.,Eighty First Hospital of Peoples Liberation Army | Wan Z.,Nantong University | And 4 more authors.
BioMed Research International | Year: 2014

Aim. To investigate the role and mechanism of miR-15b in the proliferation and apoptosis of glioma. Methods. The miR-15b mimics were transfected into human glioma cells to upregulate the miR-15b expression. Cyclin D1 was determined by both western blotting analysis and luciferase reporter assay. Methylthiazol tetrazolium (MTT) and flow cytometry were employed to detect the cell proliferation, cell cycle, and apoptosis. Results. Overexpression of miR-15b inhibits proliferation by arrested cell cycle progression and induces apoptosis, possibly by directly targeting Cyclin D1. Both luciferase assay and bioinformatics search revealed a putative target site of miR-15b binding to the 3′-UTR of Cyclin D1. Moreover, expression of miR-15b in glioma tissues was found to be inversely correlated with Cyclin D1 expression. Enforced Cyclin D1 could abrogate the miR-15b-mediated cell cycle arrest and apoptosis. Conclusions. Our findings identified that miR-15b may function as a glioma suppressor by targeting the Cyclin D1, which may provide a novel therapeutic strategy for treatment of glioma. © 2014 Guan Sun et al.

Wang W.,Nanjing Medical University | Xu D.,Nanjing Medical University | Wang B.,Qingdao University | Yan S.,Nanjing Medical University | And 5 more authors.
Mediators of Inflammation | Year: 2015

Gout is a common inflammatory disease characterized by acute arthritis and hyperuricemia. A number of epidemiological studies have suggested the critical role of gout in carcinogenesis. The aim of this study was to estimate the association between gout and cancer risk by meta-analysis of all relevant studies published to date. A comprehensive literature search in PubMed and Embase databases from their inception up to July 1, 2014, was performed to identify eligible studies. The strength for relationship between gout and the risk of different cancers was evaluated by calculating pooled relative risks (RRs) with 95% confidence intervals (95% CIs). All analyses were carried out by STATA 12.0 software. Gout patients were at an increased risk of cancer, particularly urological cancers, digestive system cancers, and lung cancer. No such significant association between gout and the risk of breast or brain cancers was observed. Sensitivity analysis did not materially alter the pooled results. Gout is a risk factor of cancer, particularly that of urological cancers, digestive system cancers, and lung cancer. The pooled data further support the hypothesis of a link between gout and carcinogenesis. © 2015 Weijie Wang et al.

Sun G.,Nantong University | Yan S.-S.,Eighty First Hospital of Peoples Liberation Army | Shi L.,Jiangsu University | Wan Z.-Q.,Nantong University | And 4 more authors.
Molecular Medicine Reports | Year: 2016

Gliomas are the most common type of malignant brain tumor. Studies have identified that MIR-15b is negatively correlated with cripto-1 expression in glioma cells, and these molecules serve an important role in cancer development and progression. The current study was undertaken to further examine the association between these two molecules. Fluorescent quantitative PCR confirmed that MIR-15b expression was significantly downregulated in glioma tissue while cripto-1 expression was significantly increased. Subsequent to transfection with MIR-15b mimics, cripto-1 expression was significantly suppressed, and dual luciferase reporter assays further demonstrated that MIR-15b regulates cripto-1 in a targeted manner. Furthermore, MIR-15b inhibited proliferation and invasion, and promoted apoptosis of glioma cells while downregulating the expression of MMP-2 and MMP-9. In contrast, cripto-1 expression had the opposite effects. Co-transfection with MIR-15b mimics and the cripto-1 overexpression vector overcame the inhibitory action of MIR-15b on cripto-1. Therefore, it is suggested that MIR-15b modulates cell growth and invasion through targeted regulation of cripto-1 expression in glioma cells. This observation may provide novel targets for the prevention and treatment of gliomas.

Xu D.,Weifang Medical University | Yan S.,Eighty first Hospital of Peoples Liberation Army | Wang H.,Nanjing Medical University | Gu B.,Nanjing Medical University | And 4 more authors.
Cellular Physiology and Biochemistry | Year: 2015

Background/Aims: Interleukin-29 (IL-29), a critical member of type III interferons (IFNs) family, has been implicated in protecting against viral infection and modulating autoimmune inflammation. Toll-like receptor 4 (TLR4) plays a crucial role in synovial inflammation and may contribute to the pathogenesis of rheumatology arthritis (RA). However, little is known about the modifying effect of IL-29 on TLR4-mediated inflammation in RA. We aim to investigate the potential association between IL-29 and TLR4 in RA. Methods: Peripheral blood mononuclear cells (PBMCs) and serum from 77 patients with RA and 70 controls were collected to determine levels of IL-29 and TLR4 mRNA by real-time polymerase chain reaction (PCR). Levels of IL-29 and TLR4 in synovial tissues and fluid from 25 RA patients and 24 controls were detected by enzyme-linked immunosorbent assay (ELISA) or western blot assay, respectively. RAW264.7 cells were stimulated by lipopolysaccharide (LPS) and/or IL-29. The production of inflammatory cytokines including IL-6, IL-8 as well as TNF-α and the activation of nuclear factor-B (NF-κB) signaling were determined. Results: In comparison with controls, increased IL-29 was observed in PBMCs, synovial tissue, serum and synovial fluid of patients with RA. Besides, TLR4 was significantly elevated in PBMCs and synovium of RA patients. Moreover, IL-29 was positively associated with TLR4 in RA, suggested by Pearson's correlation analysis. When RAW264.7 cells were stimulated by LPS with or without IL-29 in vitro, IL-29 could enhance LPS-mediated TLR4 expression and the production of IL-6, IL-8 and TNF-α in RAW264.7 cells via the activation of NF-B signaling. Conclusion: The present study suggests, for the first time, that IL-29 can aggravate LPS/TLR4-mediated inflammation in RA depending on NF-B signaling activation. Copyright © 2015 S. Karger AG, Basel.

Guo J.,Nantong University | Shi L.,Jiangsu University | Li M.,Nanjing Medical University | Xu J.,Nantong University | And 3 more authors.
Tumor Biology | Year: 2014

Potential single-nucleotide polymorphisms (SNPs) of interleukin-4 receptor alpha (IL-4Rα) rs1801275 and rs1805015 have been implicated in glioma risk; however, the findings of previous published case-control studies are conflicting and inconclusive. We performed the updated metaanalysis with the aim to provide a more precise estimate for the role of interleukin-4Rα SNPs in glioma risk. The pooled odds ratios (ORs) with 95 % confidence intervals (CIs) were used to evaluate the strength of the gene association. Overall, the pooled analysis showed that the IL-4Rα rs1801275 polymorphism was associated with a decreased risk of glioma in the comparison of G vs. A (OR=0.87, 95 % CI=0.76-0.99, POR=0.041). Subgroup analysis by ethnicity revealed that the IL-4Rα rs1801275 variant G and GG + AG exerted a decreased risk effect on the development of glioma among Asians, but not Caucasians (G vs. A, OR=0.81, 95 % CI=0.69-0.95, POR=0.011; GG + AG vs. AA, OR=0.80, 95 % CI=0.66-0.96, POR=0.018). However, the IL-4Rα rs1805015 polymorphism did not modify the risk of glioma. Sensitivity analysis confirmed the reliability for all of the results.Our meta-analysis suggests that the polymorphism of IL-4Rα rs1801275 but not IL-4Rα rs1805015 plays a protective role in the glioma pathogenesis, particularly among Asians.

Yao F.,Nantong University | Yan S.,Eighty First Hospital Of Peoples Liberation Army | Wang X.,Nanjing Medical University | Shi D.,Nantong University | And 4 more authors.
Tumor Biology | Year: 2014

Previous case-control studies on the association of interleukin-17F (IL-17F) T7488C polymorphism and cancer risk have yielded conflicting and inconclusive findings. We performed a meta-analysis by pooling all currently available data to acquire a more precise estimation of the association. A comprehensive literature screening from the PubMed, Embase, Web of Science, and Wanfang databases was performed for eligible publications without language restrictions. The pooled odds ratios (ORs) with corresponding 95 % confidence intervals (95 % CIs) were calculated. According to the inclusion criteria, a total of nine case-control studies with 3,034 cases and 3,694 controls were included. Overall, the pooled ORs showed that IL-17F T7488C polymorphism was associated with neither increased nor decreased risk of cancer. However, the IL-17F T7488C polymorphism exerted risk effect on cancer in population-based case-control studies when stratifying analysis by source of controls (C vs T OR = 1.24, 95 % CI, 1.10–1.40, pooled OR (POR) < 0.001; TC vs TT OR = 1.28, 95 % CI, 1.11–1.48, POR = 0.001; CC + TC vs TT OR = 1.29, 95 % CI, 1.12–1.48, POR < 0.001). Additionally, the variant genotypes of IL-17F T7488C could alter the risk of gastric cancer under the following comparisons (C vs T OR = 1.29, 95 % CI, 1.13–1.47, POR < 0.001; TC vs TT OR = 1.35, 95 % CI, 1.14–1.60, POR < 0.001; CC + TC vs TT OR = 1.35, 95 % CI, 1.15–1.58, POR < 0.001). Sensitivity analysis by sequential omission of single study did not materially alter the pooled findings. The present meta-analysis suggests that the IL-17F T7488C polymorphism may modify the risk of cancer, particularly gastric cancer. However, the precise association needs to be elucidated by more individual studies with sufficient statistical power. © 2014, International Society of Oncology and BioMarkers (ISOBM).

Sun G.,Nantong University | Yan S.,Eighty First Hospital of Peoples Liberation Army | Shi L.,Jiangsu University | Wan Z.,Nantong University | And 3 more authors.
Cancer Biotherapy and Radiopharmaceuticals | Year: 2015

MicroRNA-15b (miR-15b) has been demonstrated to suppress proliferation by arresting cell cycle progression and inducing apoptosis in glioma cells. However, the prognostic value of miR-15b expression in human gliomas remains unclear. In the present study, the authors examined the expression profile in glioma specimens and the prognostic value of miR-15b in patients with gliomas. Real-time polymerase chain reaction assay was employed to detect the expression levels of miR-15b in 92 glioma tissues categorized by World Health Organization (WHO) histopathological grades. However, the prognostic value of miR-15b in human glioma has not been evaluated yet. MiR-15b expression in human glioma tissues was distinctly lower than in normal brain tissues. Furthermore, the expression of miR-15b notably decreased with the ascending histopathological grade of gliomas. Additionally, Kaplan-Meier survival analysis showed that low miR-15b expression was associated with poor overall survival in patients with gliomas. Similarly, miR-15b reduction occurred with increasing frequency in glioma patients with lower Karnofsky performance scale (KPS) scores than in those with higher KPS scores. No significant difference was observed between miR-15b expression and gender, age, and tumor location. These findings revealed that a lower expression level of miR-15b was closely related to a shorter overall survival, suggesting that miR-15b could be an intrinsic factor that plays an important role in the malignant progression of gliomas. © Mary Ann Liebert, Inc. 2015.

Yan S.,Eighty First Hospital of Peoples Liberation Army | Yan S.,Nanjing Medical University | Zhang P.,Peoples Hospital of Rizhao | Liu Y.,Peoples Hospital of Rizhao | And 6 more authors.
Mediators of Inflammation | Year: 2015

SUA is a potent antioxidant and thus may play a protective role against cancer. Many epidemiological studies have investigated this hypothesis but provided inconsistent and inconclusive findings. We aimed to precisely elucidate the association between SUA levels and cancer by pooling all available publications. Totally, 5 independent studies with 456,053 subjects and 12 with 632,472 subjects were identified after a comprehensive literature screening from PubMed, Embase, and Web of Science. The pooled RRs showed that individuals with high SUA levels were at an increased risk of total cancer incidence (RR=1.03, 95% CI 1.01-1.05, P=0.007). Positive association between high SUA levels and total cancer incidence was observed in males but not females (for men: RR=1.05, 95% CI 1.02-1.08, P=0.002; for women, RR=1.01, 95% CI 0.98-1.04, P=0.512). Besides, high SUA levels were associated with an elevated risk of total cancer mortality (RR=1.17, 95% CI 1.04-1.32, P=0.010), particularly in females (RR=1.25, 95% CI 1.07-1.45, P=0.004). The study suggests that high SUA levels increase the risk of total cancer incidence and mortality. The data do not support the hypothesis of a protective role of SUA in cancer. © 2015 Shushan Yan et al.

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