As a member of apoptosis inhibition gene family, baculoviral IAP repeat containing 5 (BIRC5) protein acts as a survival factor in oncology through multiple ways. There are huge inconsistent results between urinary cancer risk and BIRC5 polymorphisms, so we searched and documented all eligible articles to clear up the mystery with the help of meta-analysis. According to the inclusion and exclusion criteria, we performed an overall search in Web of Science, PubMed, Google Scholar, Medline, CNKI and Wanfang database with pre-set search strategy up to November 2019. Z-test was performed to determine the statistical difference by Odds ratios (ORs) and 95% confidence intervals (CIs). The stability of the pooled ORs was conducted by one-way sensitivity analyses, Begg's funnel plots and Egger's test were employed to access the potential publication bias. The relationship of polymorphisms and BIRC5 expression was exposed by in-silico analysis, as well as the effects to tumorigenesis and prognosis. Finally, we enrolled 19 case-control studies to conducted this meta-analysis. An upgrade risk in rs9904341 of BIRC5 were revealed to be associated with urinary cancer in allele contrast model (OR = 1.222, P = 0.012), homozygote contrast model (OR = 1.579, P = 0.0001) and recessive contrast model (OR = 1.433, P < 0.001), as well as rs2071214 polymorphism in the subgroup analysis of BCa in allele contrast model (OR = 1.362, P = 0.011) and recessive contrast model (OR = 1.417, P = 0.015). On the other hand, rs17878467 variant plays an important role in prevent the tumorigenicity of urinary cancer in allele contrast model (OR = 0.672, P = 0.009), heterozygote contrast model (OR = 0.585, P = 0.006) and dominant contrast model (OR = 0.595, P = 0.004). In conclusion, we found that BIRC5 rs9904341, rs2071214 polymorphisms might cause the increased risk of urinary cancer, while rs17878467 reduces risk.

In order to investigate the biological characteristics of avian pathogenic Escherichia coli (APEC) isolated in eastern China, a total of 243 isolates were isolated from diseased poultry on different farms during the period from 2007 to 2014. These isolates were characterized for serogroups (polymerase chain reaction and agglutination), the presence of virulence-associated genes (fimC, iss, ompA, fyuA, stx2f, iroC, iucD, hlyE, tsh, cvaC, irp2, and papC) and class I integrons (polymerase chain reaction), drug susceptibilities (disk diffusion method) and the biofilm-forming abilities (semi-quantitative method). The results showed that the most predominant serogroups were O78 (87 isolates, 35.8%) and O2 (35 isolates, 14.4%). Gene profiling found that fimC and ompA were frequently distributed among the isolates and that 77.4% of the isolates were positive for class 1 integrons. Overall, isolates displayed resistance to tetracycline (97.5%), nalidixic acid (82.3%), ampicillin (81.1%), sulphafurazole (80.7%), streptomycin (79.0%), trimethoprim (78.2%) and cotrimoxazole (78.2%). Multiple-drug resistance was exhibited in 80.3% of the isolates, and the presence of class 1 integrons is associated with multidrug resistance. Finally, 151 isolates had the ability to form biofilms in vitro, and drug resistance seemed relative to biofilm-forming abilities.

ERCC4 plays an essential role in the nucleotide excision repair (NER) pathway, which is involved in the removal of a wide variety of DNA lesions. To determine whether the ERCC4 tagging SNPs (tSNPs) are associated with risk of gastric cancer, we conducted a hospital-based case-control study of 350 cases and 468 cancer-free controls. In the logistic regression (LR) analysis, we found a significantly decreased risk of gastric cancer associated with the rs744154 GC/CC genotypes [adjusted odds ratio (OR)=0.56, 95% confidence interval (CI)=0.42-0.75, false discovery rate (FDR) P=0.003] compared with the wild-type GG genotype. Haplotype-based association study revealed that the CGC haplotype that containing the rs744154 C allele can decrease the risk of gastric cancer compared with the most common haplotype GGT (adjusted OR=0.61, 95% CI=0.46-0.81). Using the multifactor dimensionality reduction (MDR) analysis, we identified that the SNP rs744154 and smoking status were the best two predictive factors for gastric cancer with a testing accuracy of 55.76% and a perfect cross-validation consistency (CVC) of 10 (P=0.001). Furthermore, the smokers with the rs744154 GC/CC genotypes showed a decreased risk of gastric cancer (adjusted OR=0.55, 95% CI=0.35-0.85) compared with the smokers with the GG genotype using multivariate LR analysis. The above findings consistently suggested that genetic variants in the ERCC4 gene may play a protective role in the etiology of gastric cancer, even in the smokers.

This study focused on mortalin expression and its relevance to the prognosis in serous ovarian carcinoma, mortalin modulated cell malignant proliferation and EMT progression via Wnt/β-Catenin signaling pathway. In this study, data obtained from Oncomine database, Cancer Cell Line Encyclopedia (CCLE) analysis and Immunohistochemical (IHC) staining was used to assess the expression of mortalin in serous ovarian carcinoma. The prognostic value of mortalin was analyzed using Meier plotter database and Kaplan-Meier. MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay, immunofluorescence (IF) staining, and colony formation assay were used to detect cell reproductive capacity. SK-OV-3 cell motility and epithelial-mesenchymal transition (EMT) were measured by wound-healing, migration and western-blot assays. Data from Oncomine showed that mortalin was highly expressed in serous ovarian carcinomas compared with corresponding normal controls. Similar results were found in CCLE analysis and in clinical specimens. High mortalin expression was associated with high histological grade and worse overall survival (OS) rate. The results of MTT analyses, IF staining, and colony formation assay indicated that MKT-077 (1-Ethyl-2-[[3-ethyl-5-(3-methyl-2(3H)-benzothiazolylidene)-4-oxo-2-thiazolidinylidene] methyl]-pyridinium chloride) suppressed the viability of SK-OV-3 cells. Besides, mortalin suppression restrained cell EMT progression by Wnt/β-Catenin signaling pathway. Taken together, mortalin is over-expressed in serous ovarian carcinoma. High mortalin expression could be a candidate for the prognostic indicator and a biomarker in serous ovarian carcinoma.