Association between XRCC3 Thr241Met polymorphism and risk of gynecological malignancies: A meta-analysis.

Studies have investigated the relationship between the X-ray cross- complementing group 3 (XRCC3) Thr241Met polymorphism and the risk of gynecological malignancies (GM) with the contradictory conclusions. Here, a meta-analysis was performed to provide clear picture of the association between Thr241Met and GM risk. The Pubmed and Chinese National Knowledge Infrastructure (CNKI) databases were searched for published eligible studies. The pooled odds ratios (OR) with their corresponding 95% confidence interval (CI) was used to assessed the strength of association. Totally, 15 publications with 5,740 cases and 9,931 controls were included. In the overall analysis, the results of meta-analysis showed no significant association between the Thr241Met and the risk of GM. However, in the Asians subgroup, significant increased risks were found in the comparisons of TT/CT+TT vs. CC(TT vs. CC: OR=3.25, 95% CI=1.47-7.18; CT+TT vs. CC: OR=1.51, 95%CI=1.10-2.09) in Asians; additionally, stratified analysis by cancer type in Asians, significantly increased risks was found in cervical carcinoma (CT vs. CC: OR=1.50, 95%CI=1.04-2.14; TT vs. CC: OR=3.14, 95%CI=1.38-7.14; CT+TT vs. CC: OR=1.64, 95% CI=1.17-2.31). It suggests that the risk of GM might be significantly increased by the XRCC3 Thr241Met polymorphism according to ethnicity and cancer types. Further studies with larger sample size in different ethnic populations and different sites of GM are needed to verify the findings.

Research on Fault Extraction Method of Variational Mode Decomposition Based on Immunized Fruit Fly Optimization Algorithm.

In recent years, a new method of fault diagnosis, named variational mode decomposition (VMD), has been widely used in industrial production, but the decomposition accuracy of VMD is determined by two parameters, which are respectively the decomposition layer number k and the penalty factor α, if the parameters are not properly selected, there will be over-decomposition or under-decomposition. In order to find an approach to determine the parameters adaptively, a method to optimize VMD by using the immune fruit fly optimization algorithm (IFOA) is proposed in this paper. In this method, permutation entropy is used as the fitness function, firstly, the immune fruit fly optimization algorithm is used to search the combined parameters of k and α in VMD, searching for the best combination parameters of k and α by iteration, and then uses the combined parameters to perform VMD, finally, the center frequency is determined through frequency spectrum analysis. The method mentioned is applied to the fault extraction of a simulated signal and a measured signal of a wind turbine gearbox, and the fault frequency is successfully extracted. Using ensemble empirical mode decomposition (EEMD) and singular spectrum decomposition (SSD) to compare with the proposed method, which validated feasibility of the proposed method.

DEP domain containing 1 suppresses apoptosis via inhibition of A20 expression, which activates the nuclear factor κB signaling pathway in HepG2 cells.

A previous study revealed that DEP domain containing 1 (DEPDC1) is involved in the carcinogenesis of bladder cancer via forming a complex with zinc finger protein 224 (ZNF224) to suppress A20 expression, resulting in the activation of the nuclear factor (NF)-κB signaling pathway; however, the role of DEPDC1 in liver cancer remains unclear. Hep G2 cells were treated with 11R-DEP: 611-628, a peptide capable of disrupting the DEPDC1-ZNF224 complex. Cell proliferation was examined using an MTT assay and apoptosis was analyzed via detection of the apoptotic marker caspase-3 using western blot analysis. A20 expression was examined via reverse transcription-quantitative polymerase chain reaction and NF-κB subcellular localization was determined via immunofluorescence staining. microRNA (miR)-130a was overexpressed in HepG2 cells and its effects on proliferation and apoptosis were examined. The results demonstrated that 11R-DEP: 611-628 (3 µM) and miR-130a inhibited cell proliferation and promoted apoptosis in HepG2 cells by activating A20 expression, which blocks the nuclear transportation of NF-κB. In addition, the results demonstrated that the 11R-DEP: 611-628 (3 µM) treatment resulted in downregulation of DEPDC1 expression, indicating that DEPDC1 expression is regulated by the DEPDC1-ZNF224 complex. In conclusion, the data indicated that DEPDC1 suppresses apoptosis to promote cell proliferation through the NF-κB signaling pathway in HepG2 cells and that DEPDC1 is a potential target for the treatment of liver cancer.

Association between miR-199a rs74723057 and MET rs1621 polymorphisms and the risk of hepatocellular carcinoma.

MicroRNAs (miRNAs) can regulate gene expression at post-transcriptional levels, thereby influence cancer risk. The aim of the current study is to investigate association between miR-199a rs74723057 and MET rs1621 and HCC risk in 1032 HCC patients and 1060 cancer-free controls. These two SNPs were genotyped by using the Agena MassARRAY genotyping system. Odds ratio (OR) and 95% confidence interval (95%CI) were calculated to assess the strength of the associations. We found that compared with the wild-type AA genotype of MET rs1621, the variant GG genotype was associated with a decreased risk for HCC (OR = 0.24, 95% CI = 0.06-0.96, P = 0.043). No association between miR-199a rs74723057 and HCC risk was observed. In addition, an interaction effect on HCC risk between the selected two SNPs was found. Among those who carried the CG/GG genotypes of miR-199a rs74723057, those who carried the GG genotype of MET rs1621 had a reduced risk of HCC, when compared with those who carried the AG/AA genotypes of MET rs1621 (OR = 0.15, 95% CI = 0.03~0.73, P for interaction = 0.018). Our results suggest that MET rs1621 polymorphism, alone and combined with miR-199a rs74723057, may influence susceptibility to HCC. Further large-scale association studies and functional studies are needed to validate our findings.