Bisphenol A (BPA) can accumulate in the human body and promote the progression of various cancers. However, its role in the development of neuroblastoma (NB) is largely unknown. Our present study revealed that nanomolar concentrations of BPA can significantly increase the proliferation, migration and invasion of NB SH-SY5Y and SiMa cells, further evidenced by the upregulation of human proliferating cell nuclear antigen, Bcl-2, vimentin and fibronectin. Real-time PCR and ELISA results suggested that nanomolar BPA can increase the expression of interleukin-6 (IL-6), but had no effect on the expression of IL-2, IL-8, IL-10 or IL-12. The neutralization antibody of IL-6 can abolish BPA-induced proliferation and invasion of NB cells. The inhibitor of NF-κB (BAY 11-7082), but not PD98059 (PD, ERK1/2 inhibitor) or LY294002 (LY, PI3 K/Akt inhibitor), attenuated BPA-induced IL-6 expression and cell proliferation and invasion. In addition, BPA treatment also rapidly increased the phosphorylation of p65 since treatment for 5 min. Collectively, our data revealed that nanomolar BPA can trigger the malignancy of NB cells via activation of NF-κB/IL-6 signals, suggesting that more attention should be paid to the potential health risks of daily BPA intake.
The aim of this study was to investigate the association between single-nucleotide polymorphisms (SNP) within MEFV gene and Henoch-Schönlein purpura (HSP) risk, and the impact of SNP-SNP interaction on HSP risk in Chinese children. A total of 662 subjects with a mean age of 7.9 ± 2.4 years old were selected, including 320 HSP patients and 342 normal controls. Logistic regression was performed to investigate association between SNP and HSP risk, and generalized multifactor dimensionality reduction (GMDR) was used to analyze the SNP-SNP interaction. Logistic analysis showed a significant association between genotypes of variants in rs3743930 and increased HSP risk. The carriers of homozygous mutant of rs3743930 polymorphism revealed increased HSP risk than those with wild-type homozygotes; OR (95% CI) was 1.55 (1.23-1.85). GMDR analysis suggested a significant two-locus model (p = 0.0107) involving rs3743930 and rs28940580, indicating a potential SNP-SNP interaction between rs3743930 and rs28940580. Overall, the two-locus models had a cross-validation consistency of 10 of 10 and had the testing accuracy of 60.72%. Subjects with rs3743930-GC or CC and rs28940580-GA or AA genotype have the highest HSP risk, compared to subjects with rs3743930-GG and rs28940580-GG genotype; OR (95% CI) was 2.13 (1.52-2.89). The variants in rs3743930 and interaction between rs3743930 and rs28940580 were associated with increased HSP risk in Chinese children.
Aims The association of single nucleotide polymorphisms (SNPs) of glutamate receptor 2 (GRIK2) gene, as well as gene‐gene interaction with the risk of early‐onset epilepsy susceptibility, was studied in Chinese children. Methods Generalized multi‐factor dimension reduction (GMDR) is used to identify the optimal linkage between interaction among four SNPs and early‐onset epilepsy susceptibility. Logistic regression was performed to assess association between four SNPs within GRIK2 gene and the risk of epilepsy. Results The results show that the risk of epilepsy in the rs4840200‐T allele carriers was significantly higher than CC (CT/TT vs CC), adjusted OR (95% CI) = 1.74 (1.31‐2.20), and the carrier of rs3213607‐A allele was also higher than CC (CG/GG vs CC) with adjusted OR (95% CI) = 1.61 (1.23‐2.10). We did not detect significant association between rs9390754 and rs2235076 within GRIK2 gene and epilepsy risk. In the GMDR analysis for the gene/gene interaction (2‐4 locus models), we found a significant two‐locus model (P = 0.001) involving rs4840200 and rs9390754. The cross‐validation consistency was 10/10, and the prediction error was 0.632. Participants with rs4840200‐CT/TT and rs9390754‐GA/AA genotype within GRIK2 gene have the highest epilepsy risk, compared to participants with rs4840200‐CC and rs9390754‐GG genotype within GRIK2 gene, OR (95% CI) = 2.42 (1.78‐3.11), after covariates adjustment for age and gender. Conclusions Both rs4840200‐T and rs3213607‐A, and the interactions between rs4840200 and rs9390754 are related to the increased risk of epilepsy risk.
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