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Abstract
BMAL1 knockdown resulted in increased AKT/mTOR activation across all examined colorectal cancer cell lines.
- Different colorectal cancer cell lines responded uniquely to BMAL1 knockdown.
- HCT116 cells underwent apoptosis with reduced P53 activation and increased AKT/mTOR activation, leading to higher proliferation.
- SW480 cells exhibited moderate P53 and mTOR activation, resulting in cell senescence.
- SW620 cells showed faster growth with increased AKT activation but unchanged mutant P53 activation.
- BMAL1 knockdown affected P53 activation differently depending on the cellular context, influencing colorectal cancer cell fates.
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