ArticleCancer research2011
RNA helicase DDX5 is a p53-independent target of ARF that participates in ribosome biogenesis.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 75 citations in OpenAlex.
- Mechanobiology of the Nucleolus.Biology of the cell · 2026Review
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- Unwinding new therapeutic opportunities in rhabdomyosarcoma: the role of RNA helicase DDX5.Frontiers in cell and developmental biology · 2025Review
- Elevated Type I Interferon Signaling Defines the Proliferative Advantage of ARF and p53 Mutant Tumor Cells.Molecular and cellular biology · 2025Article
- Diverse functions of DEAD-box proteins in oligodendrocyte development, differentiation, and homeostasis.Journal of neurochemistry · 2025Review
- DEAD/H Box 5 (DDX5) Augments E2F1-Induced Cell Death Independent of the Tumor Suppressor p53.International journal of molecular sciences · 2024Article
- DDX5 promotes esophageal squamous cell carcinoma growth through sustaining VAV3 mRNA stability.Oncogene · 2024Article
- Fragile X Messenger Ribonucleoprotein Protein and Its Multifunctionality: From Cytosol to Nucleolus and Back.Biomolecules · 2024Review
- Review
- DEAD-box RNA helicases with special reference to p68: Unwinding their biology, versatility, and therapeutic opportunity in cancer.Genes & diseases · 2023Review
- Ribosome biogenesis factors-from names to functions.The EMBO journal · 2023Review
- FL118, acting as a 'molecular glue degrader', binds to dephosphorylates and degrades the oncoprotein DDX5 (p68) to control c-Myc, survivin and mutant Kras against colorectal and pancreatic cancer with high efficacy.Clinical and translational medicine · 2022Article
- Synthetic lethal interactions of DEAD/H-box helicases as targets for cancer therapy.Frontiers in oncology · 2022Review
- Pan-cancer analysis of the prognostic and immunological roles ofFrontiers in genetics · 2022Article
- DDX5 and DDX17-multifaceted proteins in the regulation of tumorigenesis and tumor progression.Frontiers in oncology · 2022Review
- It's Getting Complicated-A Fresh Look at p53-MDM2-ARF Triangle in Tumorigenesis and Cancer Therapy.Frontiers in cell and developmental biology · 2022Review
- LncRNA Platr22 promotes super-enhancer activity and stem cell pluripotency.Journal of molecular cell biology · 2021Article
- RNA helicase DDX5 acts as a critical regulator for survival of neonatal mouse gonocytes.Cell proliferation · 2021Article
- Characterization of R-Loop-Interacting Proteins in Embryonic Stem Cells Reveals Roles in rRNA Processing and Gene Expression.Molecular & cellular proteomics : MCP · 2021Article
- Dysregulated gene-associated biomarkers for Alzheimer's disease and aging.Translational neuroscience · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The p19ARF tumor suppressor limits ribosome biogenesis and responds to hyperproliferative signals to activate the p53 checkpoint response. Although its activation of p53 has been well characterized, the role of ARF in restraining nucleolar ribosome production is poorly understood. Here we report the use of a mass spectroscopic analysis to identify protein changes within the nucleoli of Arf-deficient mouse cells. Through this approach, we discovered that ARF limited the nucleolar localization of the RNA helicase DDX5, which promotes the synthesis and maturation of rRNA, ultimately increasing ribosome output and proliferation. ARF inhibited the interaction between DDX5 and nucleophosmin (NPM), preventing association of DDX5 with the rDNA promoter and nuclear pre-ribosomes. In addition, Arf-deficient cells transformed by oncogenic RasV12 were addicted to DDX5, because reduction of DDX5 was sufficient to impair RasV12-driven colony formation in soft agar and tumor growth in mice. Taken together, our findings indicate that DDX5 is a key p53-independent target of the ARF tumor suppressor and is a novel non-oncogene participant in ribosome biogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.