Identification of four novel prognosis biomarkers and potential therapeutic drugs for human colorectal cancer by bioinformatics analysis

Colorectal cancer(CRC)is one of the most deadly cancers in the world with few reliable biomarkers that have been selected into clinical guidelines for prognosis of CRC patients.In this study,mRNA microarray datasets GSE113513,GSE21510,GSE44076,and GSE32323 were obtained from the Gene Expression Omnibus(GEO)and analyzed with bioinformatics to identify hub genes in CRC development.Differentially expressed genes(DEGs)were analyzed using the GEO2 R tool.Gene ontology(GO)and KEGG analyses were performed through the DAVID database.STRING database and Cytoscape software were used to construct a protein-protein interaction(PPI)network and identify key modules and hub genes.Survival analyses of the DEGs were performed on GEPIA database.The Connectivity Map database was used to screen potential drugs.A total of 865 DEGs were identified,including 374 upregulated and 491 downregulated genes.These DEGs were mainly associated with metabolic pathways,pathways in cancer,cell cycle and so on.The PPI network was identified with 863 nodes and 5817 edges.Survival analysis revealed that HMMR,PAICS,ETFDH,and SCG2 were significantly associated with overall survival of CRC patients.And blebbistatin and sulconazole were identified as candidate drugs.In conclusion,our study found four hub genes involved in CRC,which may provide novel potential biomarkers for CRC prognosis,and two potential candidate drugs for CRC.

Smurfs have“fused”into the asymmetric division of stem cells

The asymmetric cell division is the way in which a stem cell divides into one daughter stem cell and one differentiated daughter cell.This process is one of the key principles of developmental biology that ensures the perpetual supply of stem cells while allowing a particular cell lineage to be populated.During Drosophila oogenesis,the fate of the daughter stem cell produced from the asymmetric division of germline stem cells(GSCs)is specified by Decapentaplegic(Dpp),but the other daughter cell has almost equal access to the Dpp signal.How Dpp signaling is inactivated in the differentiated daughter cell has been a deep mystery until a recent study,led by Dahua Chen of the Institute of Zoology,China(Xia et al.,2010),showed that the Dpp receptor,Thick vein(Tkv),is degraded specifically in the differentiated daughter cell by an HECT-domain ubiquitin E3 ligase,Smurf,in conjunction with a serine-threonine kinase Fused(Fu).This finding is as much revealing as it is surprising,because up until now Fu is considered a core member of the Hedgehog signaling pathway.