Bortezomib Potentiates the Effect of Roscovitine Via Dna Damage Induced Apoptosis in A549 Lung Cancer Cells

The adoption of new treatment modalities remains crucial as lung cancer has one the lowest survival rates, along with liver and pancreatic cancer. Bortezomib is a proteasome inhibitor that higher anticancer effect in combination therapies. Therefore, aim this study to investigate whether bortezomib could have additional when combined cyclin-dependent kinase (CDK) inhibitor-roscovitine vitro. Apoptosis related gene expression levels p53, Noxa, Puma, Bcl-xL, Bak, Casp-3 Casp-7 were measured by quantitative PCR (qPCR) upon 10-20μM roscovitine 30nM for 24 hours. Synergistic on apoptosis was also investigated at protein analyzing Cleaved Parp expressions. Induction autophagy determined western blotting B-catenin LC3B I-II. Roscovitine induced upregulating p53 pathway its downstream mediators. increased Caspase3 cleavage significantly 24h. inhibited triggered induction 48hours. As cells evade programmed cell death, CDK inhibitors might be used direct into apoptosis. This concludes potentiates via DNA damage A549 cells.