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    the mitochondrial genome expansion and shrinkage events, might be related to CMS. Additionally, the candidate protein-coding genes and CMS-specific ORFs were closely associated with the CMS mechanism. Verification experiments of one of the candidate genes were performed, and the validity of our research results was supported. Copyright © 2020 Wang, Cai, Hu, Li, Fan, Tan, Liu and Zhou.Using calibrations to obtain absolute divergence times is standard practice in molecular clock studies. While the use of primary (e.g., fossil) calibrations is preferred, this approach can be limiting because of their rarity in fast-growing datasets. Thus, alternatives need to be explored, such as the use of secondary (molecularly-derived) calibrations that can anchor a timetree in a larger number of nodes. However, the use of secondary calibrations has been discouraged in the past because of concerns in the error rates of the node estimates they produce with an apparent high precision. Here, we quantify the amount of errors in estimates produced by the use of secondary calibrations relative to true times and primary calibrations placed on distant nodes. We find that, overall, the inaccuracies in estimates based on secondary calibrations are predictable and mirror errors associated with primary calibrations and their confidence intervals. Additionally, we find comparable error rates in estimated times from secondary calibrations and distant primary calibrations, although the precision of estimates derived from distant primary calibrations is roughly twice as good as that of estimates derived from secondary calibrations. This suggests that increasing dataset size to include primary calibrations may produce divergence times that are about as accurate as those from secondary calibrations, albeit with a higher precision. Overall, our results suggest that secondary calibrations may be useful to explore the parameter space of plausible evolutionary scenarios when compared to time estimates obtained with distant primary calibrations. Copyright © 2020 Powell, Waskin and Battistuzzi.Autophagy is a self-degradation process that maintains homeostasis against stress in cells. Autophagy dysfunction plays a central role in the development of tumors, such as colorectal cancer (CRC). In this study, autophagy-related differentially expressed genes, their downstream functions, and upstream regulatory factors including RNA-binding proteins (RBP) involved in programmed cell death in the CRC were investigated. Transcription factors (TFs) and miRNAs have been shown to mainly regulate autophagy genes. Interestingly, we found that some of the RBP in the CRC, such as DDX17, SETDB1, and POLR3A, play an important regulatory role in maintaining autophagy at a basal level during growth by acting as TFs that regulate autophagy. Promoter methylations showed negative regulations on differentially expressed autophagy gene (DEAG), while copy number variations revealed a positive role in them. A proportional hazards regression analysis indicated that using autophagy-related prognostic signature can divide patients into high-risk and low-risk groups. A-1331852 datasheet Autophagy associated FDA-approved drugs were studied by a prognostic network. This would contribute to the identifications of new potential molecular therapeutic targets for CRC. Copyright © 2020 Zhang, Jiang, Wang, Zheng, Xu, Qi, Huang, Lu, Li and Wang.Background Upregulation of the six-transmembrane epithelial antigen of prostate-1 (STEAP1) is closely associated with prognosis of numerous malignant cancers. However, its role in lung adenocarcinoma (LUAD), the most common type of lung cancer, remains unknown. This study aimed to investigate the role of STEAP1 in the occurrence and progression of LUAD and the potential mechanisms underlying its regulatory effects. Methods STEAP1 mRNA and protein expression were analyzed in 40 LUAD patients via real-time PCR and western blotting, respectively. We accessed the clinical data of 522 LUAD patients from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) to investigate the expression and prognostic role of STEAP1 in LUAD. Further, we performed gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and gene set enrichment analysis (GSEA) to elucidate the potential mechanism underlying the role of STEAP1 in LUAD. The protein-protein interaction (PPI) network of STEAP1 STEAP1 upregulation potentially influences the occurrence and progression of LUAD and its co-expressed genes via regulation of homologous recombination, p53 signaling, cell cycle, DNA replication, and apoptosis. STEAP1 is a potential prognostic biomarker for LUAD. Copyright © 2020 Guo, Ke, Liu, Gao, Fang, Chen, Song, Han, Lu and Xu.The profiling of DNA methylation modifications in peripheral blood has significant potential to determine risk factors for human disease. Little is known concerning the sensitivity of DNA methylation profiles to ex vivo sample handling. Here, we studied typical conditions prior to sample storage associated with cord blood samples obtained from clinical investigations using reduced representation bisulfite sequencing. We examined both whole blood collected shortly after birth and dried blood spots, a potentially important source of neonatal blood for investigation of the DNA methylome and the Developmental Origins of Health and Disease in human cohorts because they are routinely collected during clinical care. Samples were matched across different time conditions, as they were from the same cord blood samples obtained from the same individuals. Maintaining whole blood ex vivo up to 24 h (4°C) or dried blood spots up to 7 days (room temp.) had little effect on DNA methylation profiles. Minimal differences were detected between cord blood immediately frozen and dried blood spots. Our results indicate that DNA methylation profiles are resilient to ex vivo sample handling conditions prior to storage. These data will help guide future human studies focused toward determination of DNA methylation modifications in whole blood. Copyright © 2020 Sasaki, Kim, Murphy and Matthews.

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