The IL-4, IL-4 receptor (IL4R), and IL-13 genes are crucial immune factors and may influence the course of various diseases. In the present study, we investigated the association between the potential functional polymorphisms in IL-4, IL-4R, and IL-13 and coal workers' pneumoconiosis (CWP) risk in a Chinese population.
Objective: To investigate the apoptosis induced by Sapindus Saponin(SPSP) in human lung cancer cell A549 and its molecular mechanisms. Methods: Using MTT assay, the inhibition of SPSP on the proliferation of A549 cells was detected;changes of the cell morphology and effects on apoptosis were observed by Hoechst 33258 and flow cytometry; real time PCR was used to detect m RNA expressions of bcl-2. Results: SPSP significantly inhibited the growth of A549 cells in a dose-de-pendent manner. The test of Hoechst 33258 and flow cytometry indicated that SPSP could induce the apoptosis of A549 cells.Real time PCR indicated that SPSP could obviously decrease the expression of bcl-2. Conclusion: SPSP could promote the apoptosis of A549 cells, which may be related to the decrease of bcl-2 expression.
Raf-1 kinase inhibitor protein (RKIP) plays a critical role in tumor development by regulating cell functions such as invasion, apoptosis and differentiation. Down-regulation of RKIP expression has been implicated in the development and progression of renal cell carcinoma (RCC). Herein, we hypothesized that genetic polymorphisms in RKIP might be associated with susceptibility and progression of RCC.A total of 5 tagging single-nucleotide polymorphisms (tSNPs) in RKIP were selected and genotyped by SNapShot method in a case-control study of 859 RCC patients and 1004 controls. The logistic regression was used to evaluate the genetic association with occurrence and progression of RCC. The functionality of the important SNP was preliminary examined by qRT-PCR.We found that the rs17512051 in the promoter region of RKIP was significantly associated with decreased clear cell RCC (ccRCC) risk (TA/AA vs. TT: P = 0.039, OR = 0.78, 95%CI = 0.62-0.99). Another SNP (rs1051470) in the 3'UTR region of RKIP was marginally associated with increased ccRCC risk (TT vs. CC+CT: OR = 1.45, 95%CI = 1.01-2.09). In the stratified analysis, the protective effect of rs17512051 was more predominant in the subgroups of male, non-smokers, non-drinkers as well as subjects without history of diabetes. Furthermore, we observed higher RKIP mRNA levels in the presence of the rs17512051A allele in normal renal tissues.Our results suggest that the potentially functional RKIP rs17512051 polymorphism may affect ccRCC susceptibility through altering the endogenous RKIP expression level. Risk effects and the functional impact of this polymorphism need further validation.
A polymorphism rs4938723 (T > C) within the promoter region of pri-miR-34b/c has been found to not only affect the expression of mature miR-34b/c but also contribute to the susceptibility to several cancer types. We designed a case-control study to evaluate the role of rs4938723 in childhood acute lymphoblastic leukemia (ALL). The rs4938723 CC genotype was significantly associated with reduced ALL risk (p = 0.003, ORadjusted = 0.51, 95% CI = 0.33-0.80 for CC vs. TT). Stratification analyses showed the differences were pronounced in older (> 6 years), male subjects, as well as in patients in low risk and T-ALL subtypes. The in vitro luciferase assays in Jurkat and K-562 cell lines showed that the transcription activity of miR-34b/c was increased when T allele transited to C allele (p < 0.05). In conclusion, rs4938723 genetic variant contributed to the susceptibility to Chinese childhood ALL by influencing the transcription activity of miR-34b/c promoter.
Background: Long-term exposure to particular matter (PM), especially fine PM (< 2.5μm in the aerodynamic diameter, PM2.5), is associated with increased risk of cardiovascular disorders. This study aimed to evaluate the association between long-term exposure to PM2.5/PM10 and the metabolites change in the plasma. Specifically, using metabolomics we sought to identify the biomarkers for the vulnerable subgroup to PM2.5 exposure.
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