Year: 2007
Type: review
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 coactivator 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.
Source: Cell Cycle
DOI: 10.4161/cc.6.22.4895
Authors: Mu-Shui Dai, Rosalie Sears, Hua Lu
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: G1121795095, G1167304939, Dissection of the feedback inhibition of c-Myc by L11, Integration of Ras, Myc and E2F Signaling Pathways, Study of a FACTp140-SSRP1-associated p53 Kinase, G221847286, Dissection of the feedback inhibition of c-Myc by L11, G3770099111, G5296496745, Molecular Dissection of a Novel P53-like Protein, G6195694424, The Role of Ribosomal Proteins in the P53-MDM2 Pathway, G650070032, Cellular Mechanisms Controlling Myc Protein Stability
OpenAlex ID: W2055078106