Cancers, Journal Year: 2025, Volume and Issue: 17(10), P. 1597 - 1597
Published: May 8, 2025
The tumor suppressor protein p53 prevents the malignant transformation of cells by responding to DNA damage, oncogene activation, and abnormal growth signals including ribosome assembly defects. Under normal conditions, activity is controlled regulatory proteins MDM2 MDM4, which suppress its function through ubiquitin-mediated degradation transcriptional inhibition. A subset ribosomal initiates response impaired biogenesis. ability some control MDM4 activities, thereby p53, underscores an intriguing aspect cell biology: primarily known for their roles in can exert extra-ribosomal functions. One notable example cellular RNA-protein complex involving RPL5, RPL11, 5S rRNA (5S RNP) inhibits stabilizes p53. Another RP, RPL22, frequently mutated cancers with microsatellite instability paralog RPL22L1 often amplified. Recent studies have revealed that RPL22 directly modulates alternative splicing promote suggesting protein-p53 relationship more than previously thought. Cellular responses biogenesis inhibition extend beyond general alterations transcription translation actively determine cancer fate selectively engaging tumor-suppressor pathways. RPL22’s effect on other mRNA events a striking example. better understanding mechanisms involved could guide development improved treatments.
Language: Английский