Feedback regulation of c-Myc by ribosomal protein L11

Research output: Contribution to journalReview article

33 Scopus citations

Abstract

Several ribosomal proteins including L11 have been shown to activate p53 by inhibiting oncoprotein MDM2, leading to inhibition of cell cycle progression. Our recent study showed that L11 also inhibits oncoprotein c-Myc. Overexpression of L11 inhibits c-Myc-induced transcription and cell proliferation, while reduction of endogenous L11 increases these c-Myc activities. Interestingly, L11 is a transcriptional target of c-Myc, thus forming a negative feedback loop. We further showed that L11 competes with co-activator TRRAP for binding to c-Myc through the Myc box II (MB II) and reduces histone H4 acetylation at c-Myc target gene promoters. In addition, L11 appears to regulate c-Myc levels. Knocking down L11 markedly increases the mRNA and protein levels of endogenous c-Myc. These results suggest that L11 also inhibits cell cycle progression by regulating the c-Myc pathway. Here we further discuss the implications of this regulation and questions that this finding raises.

Original languageEnglish (US)
Pages (from-to)2735-2741
Number of pages7
JournalCell Cycle
Volume6
Issue number22
DOIs
StatePublished - Nov 15 2007

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Keywords

  • Cell cycle
  • L11
  • Ribosomal protein
  • TRRAP
  • Transcription
  • c-Myc

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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