NOP56 Drives Colorectal Cancer Progression by Modulating p53 Acetylation through SIRT1/p300 - PubMed
4 hours ago
- #p53 Acetylation
- #NOP56
- #Colorectal Cancer
- NOP56 expression is increased in colorectal cancer tissues and associated with poor patient survival.
- Silencing NOP56 suppresses cell viability, colony formation, and migration, especially in p53 wild-type cells.
- NOP56 depletion leads to cell cycle arrest and apoptosis by increasing p53 and p21 levels and reducing pro-caspase-3, c-Myc, and other factors.
- NOP56 promotes p53 degradation, while its knockdown enhances p53 stability and acetylation via the SIRT1/p300 axis.
- NOP56 silencing enhances the cytotoxic effect of 5-fluorouracil (5-FU) in vitro.
- In xenograft models, NOP56 knockdown reduces tumor growth, PCNA, and SIRT1 expression, and increases p53 and cleaved caspase-3 levels.
- NOP56 is identified as an oncogenic driver in CRC, with inhibition triggering apoptosis through p53 acetylation, making it a potential therapeutic target.