Mutant Kras- and p16-Regulated NOX4 Activation Overcomes Metabolic Checkpoints in Development of Pancreatic Ductal Adenocarcinoma

That mutational activation of Kras and inactivation of p16 are two signature genetic alterations required for development of PDAC. To elucidate the downstream pathways activated by oncogenic Kras and inactivated p16 in human pancreatic tumorigenesis, we profiled gene expression in HPNE/Kras/shp16 and HPNE/Kras cells using cDNA microarray analysis. We performed cDNA microarray analysis to compare p16 stably silencing cell line originating from HPNE cells with mutant Kras (HPNE/Kras/shp16). HPNE/Kras/shp16 cells placed in the reference channel in hybridization. Expression profiling by array. Two-condition experiment, HPNE/Kras vs. HPNE/Kras/shp16 cells.