ReviewBiochimica et biophysica acta2016
TIF-IA: An oncogenic target of pre-ribosomal RNA synthesis.
Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Signaling to make human ribosomes: Connections between the cytoplasm and the nucleolus.Molecular cell · 2026Review
- Clinical significance and functional characterization of RRN3 in gastric cancer: insights from pan-cancer analysis and experimental validation.Frontiers in oncology · 2026Article
- Nutrient stress diverts RRN3 from rRNA transcription to alternative polyadenylation of autophagy mRNAs in ovarian cancer.Cell death & disease · 2025Article
- Molecular basis of CX-5461-induced DNA damage response in primary vascular smooth muscle cells.Heliyon · 2024Article
- High RRN3 expression is associated with malignant characteristics and poor prognosis in pancreatic cancer.International journal of clinical oncology · 2023Article
- The homeostatic regulation of ribosome biogenesis.Seminars in cell & developmental biology · 2023Review
- Analysis and identification of mMolecular therapy. Nucleic acids · 2022Article
- Regulation of Nucleolar Activity by MYC.Cells · 2022Review
- The NF-κB Nucleolar Stress Response Pathway.Biomedicines · 2021Review
- Molecular Regulation of Skeletal Muscle Growth and Organelle Biosynthesis: Practical Recommendations for Exercise Training.International journal of molecular sciences · 2021Review
- Leflunomide Suppresses the Growth of LKB1-Inactivated Tumors in the Immune-Competent Host and Attenuates Distant Cancer Metastasis.Molecular cancer therapeutics · 2021Article
- Article
- Review
- Identification of a novel TIF-IA-NF-κB nucleolar stress response pathway.Nucleic acids research · 2018Article
- Treating hematological malignancies with drugs inhibiting ribosome biogenesis: when and why.Journal of hematology & oncology · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cancer cells devote the majority of their energy consumption to ribosome biogenesis, and pre-ribosomal RNA transcription accounts for 30-50% of all transcriptional activity. This aberrantly elevated biological activity is an attractive target for cancer therapeutic intervention if approaches can be developed to circumvent the development of side effects in normal cells. TIF-IA is a transcription factor that connects RNA polymerase I with the UBF/SL-1 complex to initiate the transcription of pre-ribosomal RNA. Its function is conserved in eukaryotes from yeast to mammals, and its activity is promoted by the phosphorylation of various oncogenic kinases in cancer cells. The depletion of TIF-IA induces cell death in lung cancer cells and mouse embryonic fibroblasts but not in several other normal tissue types evaluated in knock-out studies. Furthermore, the nuclear accumulation of TIF-IA under UTP down-regulated conditions requires the activity of LKB1 kinase, and LKB1-inactivated cancer cells are susceptible to cell death under such stress conditions. Therefore, TIF-IA may be a unique target to suppress ribosome biogenesis without significantly impacting the survival of normal tissues.
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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.