Anti-AURKA (aa 1-100) polyclonal antibody

The aim of this paper is to identify key genes in lung adenocarcinoma (LUAD) through weighted gene co-expression network analysis (WGCNA), and to further understand the molecular mechanism of LUAD. 107 gene expression profiles were downloaded from GSE10072 in the GEO database. We performed rigorous processing of the initial gene expression profile data. Subsequently, we used WGCNA to identify disease-driven modules and enforced functional enrichment analysis. The key genes were defined as the most connected genes in the driver module and were validated using the GSE75037 and TCGA database. GSE10072 removed 41 unpaired lung samples and 4 outliers. By analyzing the 62 samples using WGCNA, we obtained 26 modules and identified the brown and magenta modules as the driving modules for the LUAD. We found that the "Cell cycle", "Oocyte meiosis" and "Progesterone-mediated oocyte maturation" pathways may be related to the occurrence of LUAD. GSE75037 removed 8 outlier and obtained 2909 differentially expressed genes (DEGs), 26 genes (9 genes in the brown module, 17 genes in the magenta module) overlap with key genes in the driver module. The results of the survival analysis suggest that 19 genes were significantly correlated with the patient's survival time, including KPNA2, FEN1, RRM2, TOP2A, CENPF, MCM4, BIRC5, MELK, MAD2L1, CCNB1, CCNA2, KIF11, CDKN3, NUSAP1, CEP55, AURKA, NEK2, KIF14 and CDCA8, which may be potential biomarkers or therapeutic targets for LUAD. In this study, we provide a theoretical basis for further understanding the biological mechanism of LUAD through bioinformatics analysis of LUAD.

Aurora kinase A (AURKA) is a serine threonine kinase which affects chromosomal separation and mitotic spindle stability through interaction with the centrosome during mitosis. Two functional nonsynonymous polymorphisms of the AURKA gene (Ile31Phe and Val57Ile) have been reported recently. We analyzed the association between the two polymorphisms and risk of the occurrence of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) in the Guangxi population consisting of 348 patients with HCC and 359 control subjects, and then validated the significant association in the Guangdong population consisting of 440 cases and 456 controls. All of the participants were of Chinese origin and HBV carriers. The two polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism assay or Sequenom MassARRAY iPLEX platform. In the Guangxi population, carriers of the AURKA 31Phe allele (Ile/Phe + Phe/Phe) were significantly associated with decreased susceptibility to HBV-related HCC when compared with noncarriers (Ile/Ile) (odds ratio [OR] = 0.63, 95% confidence interval [CI] = 0.46-0.86, P = 3.4 x 10(- 3)). On the contrary, no significant association was found between Val57Ile and HBV-related HCC occurrence. The association of Ile31Phe with HBV-related HCC occurrence was confirmed in the Guangdong population (OR = 0.64, 95% CI = 0.49-0.83, P = 8.0 x 10(-4)). The pooled analysis gave a joint P value of 5.5 x 10(-6) (joint OR = 0.63, 95% CI = 0.52-0.77). Our findings suggest that AURKA Ile31Phe may play a role in mediating the susceptibility to HBV- related HCC among Chinese.