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Objective: To analyze the metastatic mechanism and its related molecular signaling pathways in the high-metastatic human lung cancer cell line SPC-A-1sci as compared with the low-metastatic human lung cancer cell line SPC-A-1 as the control, and to find the key genes for lung cancer metastasis. Methods: The differentially expressed genes between the high-metastatic human lung cancer cell line SPC-A-1sci and the low-metastatic human lung cancer cell line SPC-A-1 were detected by microarray. The potential key genes and the related signal pathways in lung cancer metastasis were examined by bioinformatics analyses including pathway analyses and signal transduction networks. Results: As compared with the SPC-A-1 cells, 2 892 genes were up-regulated and 3 248 genes were down-regulated in the SPC-A-1sci cells. There were 48 signal transduction pathways involved in the up-regulated genes and 65 signal transduction pathways involved in the down-regulated genes. The key genes in the signal transduction networks were mitogen-activated protein kinase-1, epidermal growth factor receptor, AKT 1, AKT 3, phosphoinositide-3-kinase, catalytic, delta polypeptide (PIK 3CD ), phosphoinositide-3-kinase 3, regulatory subunit1 (alpha) (PIK 3R 1), PIK 3R 3, KRAS , and insulin-like growth factor-1 receptor. Conclusion: The applications of gene chip technology and bioinformatics tools in the investigation of metastatic mechanism and its related molecular signaling pathways of high-metastatic lung cancer cell line SPC-A-1sci provide evidences for the basic research and the clinical prevention and treatment research for lung cancer metastasis. Copyright© 2012 by TUMOR.
RESUMEN
Objective To investigate the pathogenesis of familial systemic lupus erythematosus (SLE), by analyzing the gene expression profile of peripheral blood in a family with 2 SLE patients and their first-degree relatives. Methods Total RNA was extracted from peripheral blood cells of normal subjects and SLE patients. Then, synthesis double strand cDNA template from total RNA, transcription of cRNA probe with Biotin labeling, hybridization of probe with Microarray, binding of Streptavidin to Biotin, amplification with First Antibody, further amplification with Cy3-Conjugated Second Antibody, detection of Cy3 dye with ScanArray 5000 were performed. With QuantArray microarray analysis software, the scan image information was converted into numeric data. With GeneSpring microarray analysis software, cluster analysis was done to find interested genes. Results Over 3000 target genes were analysed. Fifty-nine genes differentially expressed in familial SLE patients and controls were identified. Among them, 34 genes were up-regulated and 25 genes were down-regulated. These differentially expressed genes identified in two familial SLE patients were almost identical to those found in other sporadic SLE patients. Among 34 expression increasing genes, 22 were up-regulated in SLE sisters and unaffected sisters; among 25 expression decreased genes, 17 genes down-regulated in SLE sisters and unaffected sister. Cluster analysis showed that patients were clearly separated from controls and their unaffected sisters based on their gene expression profile. These results showed that in familial SLE, multiple genes were responsible for susceptibility to SLE, and clinically unaffected relatives shared some lupus susceptibility genes with their clinically affected relatives, in addition environmental factors were probably necessary to trigger disease. Conclusion These results indicate that high-density oligonucleotide microarray has the potential to explore the heredity in SLE families.