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Abstract
Background Large scale mammalian cell culture systems, especially fed-batch systems, are currently utilised to manufacture monoclonal antibodies (MAbs) in order to meet the continuously growing global demand [1]. Nutrient deprivation and toxic metabolite accumulation commonly encountered in such systems influence the cell cycle and trigger apoptosis, resulting in shorter culture times and a lower final MAb titre. Control of the cell cycle has been previously studied in order to achieve higher titre through apoptosis inhibition by bcl-2 overexpression and cell cycle arrest in G1/G0 by p21 transfection. However, the above mentioned strategies have not always been successful; no improvement in titre was often observed though bcl-2 over-expression helped prolong the culture viability whereby the majority of cells were arrested at G1/G0 to avoid apoptosis [2-4]. Thus, a systematic insight of the dynamic relation between metabolic stress, cell cycle and apoptosis is still required. To this end, we aim to establish a novel map of the dynamic interplay between cell cycle and apoptosis at the genetic level, and provide a link with the culture conditions at the metabolic level.
Highlights
Large scale mammalian cell culture systems, especially fed-batch systems, are currently utilised to manufacture monoclonal antibodies (MAbs) in order to meet the continuously growing global demand [1]
The batch cultures started with a high fraction of cells in the G1/G0 phase, which rapidly left this state in order to join the proliferating population
The expression of casp3 followed a similar trend with a lag of few hours as its protein, caspase-3, is one of downstream targets of caspase8 and a final executor of the apoptosis pathways [6]
Summary
Large scale mammalian cell culture systems, especially fed-batch systems, are currently utilised to manufacture monoclonal antibodies (MAbs) in order to meet the continuously growing global demand [1]. Control of the cell cycle has been previously studied in order to achieve higher titre through apoptosis inhibition by bcl-2 overexpression and cell cycle arrest in G1/G0 by p21 transfection. The above mentioned strategies have not always been successful; no improvement in titre was often observed though bcl-2 over-expression helped prolong the culture viability whereby the majority of cells were arrested at G1/G0 to avoid apoptosis [2,3,4]. A systematic insight of the dynamic relation between metabolic stress, cell cycle and apoptosis is still required. To this end, we aim to establish a novel map of the dynamic interplay between cell cycle and apoptosis at the genetic level, and provide a link with the culture conditions at the metabolic level
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