ArrayExpress Uploaderarrayexpress_sidhumantreated with si-p53-#2 for 72 htreated with si-p53-#2 for 72 htreated with si-p53-#1 for 72 htreated with si-p53-#1 for 72 hcontrol siRNA for 72 hcontrol siRNA for 72 h242304In lung cancer progression, p53 mutations are more often observed in invasive tumors than in non-invasive tumors, suggesting that p53 is...E-GEOD-47436/profile/8773/arrayexpressuploader16cancergenomelunglung cancersolidDec.12, 2014FalseE-GEOD-47436_A-AFFY-44expression-data-from-immortalized-human-lung-smallExpression data from immortalized human lung small airway epithelial cellsJul.12, 2014In lung cancer progression, p53 mutations are more often observed in invasive tumors than in non-invasive tumors, suggesting that p53 is involved in tumor invasion and metastasis. To understand the nature of p53 function as a tumor suppressor, it is crucial to elucidate the detailed mechanism of the alteration in epithelial cells, the main origin of solid tumors, following p53 inactivation. To elucidate the mechanism by which p53 loss enhances invasive and motile activities in human lung small airway epithelial cells (SAECs), we performed comprehensive expression profiling analyses between p53 knockdown and control cells using GeneChip Human Genome U133 plus 2.0 arrays. SAECs were infected with lentiviruses for the expressions of CDK4 devoid of binding ability to p16INK4A, Cyclin D1 and TERT to generate immotalized SAECs. At 18 population doublings, immortalized SAECs were transfected with the siRNAs (si-control, si-p53-#1 or si-p53-#2) and used for RNA extraction and hybridization on Affymetrix microarrays.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-47436http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-47436/samples/