Objectives: Multidrug resistance (MDR) significantly reduces the efficacy of chemotherapy for lung cancer. In this study, we characterized the significance of CA916798, a gene up-regulated in cis-dichlorodiamine platinum (CDDP)-resistant lung adenocarcinoma cells, in mediating MDR in lung cancer cells. Methods: CA916798 was stably transfected into H446 cells with low endogenous expression of CA916798, and knocked down in A549/CDDP cells with high endogenous level of CA916798. Expression was confirmed by real-time PCR, Western immunoblotting and immunocytochemistry. Subsequent effects were examined on cellular growth, apoptosis and cell cycle progression. Results: Ectopic expression of CA916798 in H446 cells con... More
Objectives: Multidrug resistance (MDR) significantly reduces the efficacy of chemotherapy for lung cancer. In this study, we characterized the significance of CA916798, a gene up-regulated in cis-dichlorodiamine platinum (CDDP)-resistant lung adenocarcinoma cells, in mediating MDR in lung cancer cells. Methods: CA916798 was stably transfected into H446 cells with low endogenous expression of CA916798, and knocked down in A549/CDDP cells with high endogenous level of CA916798. Expression was confirmed by real-time PCR, Western immunoblotting and immunocytochemistry. Subsequent effects were examined on cellular growth, apoptosis and cell cycle progression. Results: Ectopic expression of CA916798 in H446 cells confered enhanced resistance to multiple chemotherapeutic agents, while its reduction rendered A549/CDDP cells less resistant to chemotherapeutic agents tested. Further analysis revealed that CA916798 regulates CDDP-induced cell growth, apoptosis and cell cycle progression. Conclusion: CA916798 may be a novel MDR-related target for lung cancer therapy.
