Lung cancer is the leading cause of cancer-related mortality in the world and NSCLC accounts for 85% of all lung cancer cases. The mainstay of treatment for patients with stage I, II and IIIA NSCLC is surgery, followed by post-operative cisplatin-based chemotherapy. Additional adjuvant therapy involving targeted tyrosine kinase inhibitors has been in use, however even for the targeted therapy, resistance eventually develops. Therefore, there is a need for identifying novel targets for this life-threatening disease. Given that preliminary studies in Ikebe lab revealed that myocardin knockdown significantly promoted caspase-3 degradation, in this study, using myocardin siRNA, we investigated the effect of the knockdown (KD) of myocardin gene on important apoptotic biomarkers such as PARP, caspase-3, and Bax; and on mitochondrial dysfunction involving respiration, and ROS formation. Our results indicated changes in the expression of multiple important apoptotic markers by myocardin knockdown in A549 NSCLC cells and myocardin knockdown was found to significantly decrease cell viability in A549 cells. Myocardin KD also showed a large, significant decrease in the maximal respiration of the cells and was found to significantly induce higher levels of ROS formation compared to the control. In summary, this study highlights myocardin as an important target in NSCLC progression and presents an interesting insight on the potential role of myocardin as a druggable target in lung adenocarcinoma. It also provides the basis for further investigation on its mechanism of apoptosis induction.

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Mitsuo Ikebe, Pierre Neuenschwander, Sakai Tsuyoshi, Qian Guoqing.


Master of Science in Biotechnology