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Enhancement of therapeutic monoclonal antibody production in CHO cells using 30Kc6 gene
Institution:1. Department of Bioengineering, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul, 04763, Republic of Korea;2. Education and Research Group for Biopharmaceutical Innovation Leader, Hanyang University, Republic of Korea;3. Department of Biomedical Engineering, Ulsan National Institute of Science and Technology (UNIST), Ulsan, 44919, Republic of Korea;4. Department of Biotechnology and Bioengineering, Kangwon National University, Chuncheon, Gangwon-do, 24341, Republic of Korea;5. Institute of Nano Science and Technology, Hanyang University, Republic of Korea;1. Department of Bioengineering, Hanyang University, 222 Wangsimri-ro, Seongdong-gu, Seoul 04763, Republic of Korea;2. BK21 Plus Future Biopharmaceutical Human Resources Training and Research Team, Hanyang University, 222 Wangsimri-ro, Seongdong-gu, Seoul 04763, Republic of Korea;3. Institute of Nano Science and Technology (INST), Hanyang University, 222 Wangsimri-ro, Seongdong-gu, Seoul 04763, Republic of Korea
Abstract:Over-expression of anti-apoptotic cloned-genes is a widely used strategy for inhibiting apoptosis in mammalian cell culture. In our previous study, we reported Bombyx mori 30K gene improved the production of recombinant proteins in Chinese hamster ovary (CHO) cells. In this study, we reengineered the CHO cells with the 30Kc6 gene and 30Kc19 gene for the production of a therapeutic monoclonal antibody (mAb) directed against the glycoprotein receptor of human platelets. After the medium was changed from serum containing one to serum-free one, expression of 30Kc6 in CHO cells increased the cell viability by 40.8% in 4 days and mAb production by 2.3-fold in 5 days. However, no significant changes in cell viability and mAb production were observed for the cells expressing 30Kc19. In the case of the cells expressing 30Kc6, the specific production rate was also improved. The expression of the 30Kc6 gene increased the cell viability and productivity because it maintained the mitochondrial membrane potential (MMP) and reduced the downstream cascade responses for apoptosis. These results indicate that 30Kc6 outperformed 30Kc19 in terms of cell death-protective capability and the production of monoclonal antibodies in CHO cells.
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