ArticleMolecular and cellular biology2012
Hypergrowth mTORC1 signals translationally activate the ARF tumor suppressor checkpoint.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- The complexity of p53-mediated metabolic regulation in tumor suppression.Seminars in cancer biology · 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
- Upregulation of 5'-terminal oligopyrimidine mRNA translation upon loss of the ARF tumor suppressor.Scientific reports · 2020Article
- Heterozygous loss of TSC2 alters p53 signaling and human stem cell reprogramming.Human molecular genetics · 2017Article
- Regulation of Cellular Metabolism and Hypoxia by p53.Cold Spring Harbor perspectives in medicine · 2016Review
- S6 Kinase- and β-TrCP2-Dependent Degradation of p19Arf Is Required for Cell Proliferation.Molecular and cellular biology · 2015Article
- ARF and p53 coordinate tumor suppression of an oncogenic IFN-β-STAT1-ISG15 signaling axis.Cell reports · 2014Article
- The ARF tumor-suppressor controls Drosha translation to prevent Ras-driven transformation.Oncogene · 2014Article
- MyoD is a tumor suppressor gene in medulloblastoma.Cancer research · 2013Article
- Metabolic regulation by p53 family members.Cell metabolism · 2013Review
- A conserved domain in exon 2 coding for the human and murine ARF tumor suppressor protein is required for autophagy induction.Autophagy · 2013Article
- Article
- HuR maintains a replicative life span by repressing the ARF tumor suppressor.Molecular and cellular biology · 2013Article
- Forget transcription: translation is where the action is.Molecular and cellular biology · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The ARF tumor suppressor is a potent sensor of hyperproliferative cues emanating from oncogenic signaling. ARF responds to these cues by eliciting a cell cycle arrest, effectively abating the tumorigenic potential of these stimuli. Prior reports have demonstrated that oncogenic Ras(V12) signaling induces ARF through a mechanism mediated by the Dmp1 transcription factor. However, we now show that ARF protein is still induced in response to Ras(V12) in the absence of Dmp1 through the enhanced translation of existing Arf mRNAs. Here, we report that the progrowth Ras/tuberous sclerosis complex (TSC)/mTORC1 signaling pathway regulates ARF protein expression and triggers ARF-mediated tumor suppression through a novel translational mechanism. Hyperactivation of mTORC1 through Tsc1 loss resulted in a significant increase in ARF expression, activation of the p53 pathway, and a dramatic cell cycle arrest, which were completely reversed upon Arf deletion. ARF protein induced from Ras(V12) in the absence of Dmp1 repressed anchorage-independent colony formation in soft agar and tumor burden in an allograft model. Taken together, our data demonstrate the ability of the ARF tumor suppressor to respond to hypergrowth stimuli to prevent unwarranted tumor formation.
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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.