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Cyclin-dependent kinases (CDKs) are highly conserved over evolutionary path and function as master regulators of the cell division cycle. Thus CDK inhibitors have been focused in the drug development for cancer and other cell proliferative disorders. Among these inhibitors Roscovitine is well known compound and under clinical trial currently while far less has been reported on another CDK inhibitor - BMI-1026, designed as a drug candidate also targeting the cell cycle. In this study we tried to define biological effects and possible mechanisms of the two chemicals by analyzing the altered transcriptome profiles when BMI-1026 and Roscovitine are applied on WI-38 cells. Our result revealed both BMI-1026 and Roscovitine produced similar gene expression profiles, where E2F target genes were suppressed in common, including cyclin A, MCM3 and PCNA along with activated p53 pathway. This finding strongly indicates that molecular machineries responsible for other established senescence models are also employed in the changes in WI-38 cells induced by the two CDK inhibitors.