ArticleMolecular and cellular biology2013
Inactivation of the mTORC1-eukaryotic translation initiation factor 4E pathway alters stress granule formation.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 82 citations in OpenAlex.
- The Role of Long Noncoding RNAs in Modulation of Stress Granules in Cancer.Journal of cellular and molecular medicine · 2026Review
- Identification of Inflammatory Markers for the Prediction and Diagnosis of Diminished Ovarian Reserve Using Olink Targeted Proteomics.Journal of clinical medicine · 2026Article
- The nuclear cap-binding complex safeguards stress-resistant protein synthesis and proliferation of stem cells.Science advances · 2026Article
- Regulation of Translation of ATF4 mRNA: A Focus on Translation Initiation Factors and RNA-Binding Proteins.Cells · 2026Review
- Stress granule dynamics govern TOR reactivation and growth recovery during post-heat stress adaptation.Science advances · 2025Article
- Lactylation of HMGB1 at K177 Drives Nuclear Export of TIAR to Promote Hypoxia-Induced Stress Granule Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cancer Cell-Secreted miR-33a Reduces Stress Granule Formation by Targeting Polyamine Metabolism in Stroma to Promote Tumourigenesis.Journal of extracellular vesicles · 2025Article
- Connecting the Dots: Stress Granule and Cardiovascular Diseases.Journal of cardiovascular translational research · 2025Review
- Aggregation of Stress Granules Induced by Hypoxia and Lipopolysaccharide via PKR-p-eIF2α Pathway and 4EBP1 Pathway Inhibits the Inflammatory Response in Peri-Implantitis.Journal of inflammation research · 2025Article
- Review
- The RNA Demethylases ALKBH5 and FTO Regulate the Translation of ATF4 mRNA in Sorafenib-Treated Hepatocarcinoma Cells.Biomolecules · 2024Article
- Stress granules affect the dual PI3K/mTOR inhibitor response by regulating the mitochondrial unfolded protein response.Cancer cell international · 2024Article
- Stress Granules as Causes and Consequences of Translation Suppression.Antioxidants & redox signaling · 2023Review
- The central role of translation elongation in response to stress.Biochemical Society transactions · 2023Article
- Stress granules: functions and mechanisms in cancer.Cell & bioscience · 2023Review
- The nuclear isoforms of the Fragile X mental retardation RNA-binding protein associate with genomic DNA bridges.Molecular biology of the cell · 2023Article
- Stress Granules in Cancer.Reviews of physiology, biochemistry and pharmacology · 2023Article
- Stress granules dynamics: benefits in cancer.BMB reports · 2022Review
- Sensitization of FOLFOX-resistant colorectal cancer cells via the modulation of a novel pathway involving protein phosphatase 2A.iScience · 2022Article
- Amyotrophic lateral sclerosis (ALS) linked mutation in Ubiquilin 2 affects stress granule assembly via TIA-1.CNS neuroscience & therapeutics · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Stress granules (SG) are cytoplasmic multimeric RNA bodies that form under stress conditions known to inhibit cap-dependent translation. SG contain translation initiation factors, RNA binding proteins, and signaling molecules. SG are known to inhibit apoptotic pathways, thus contributing to chemo- and radioresistance in tumor cells. However, whether stress granule formation involves oncogenic signaling pathways is currently unknown. Here, we report a novel role of the mTORC1-eukaryotic translation initiation factor 4E (eIF4E) pathway, a key regulator of cap-dependent translation initiation of oncogenic factors, in SG formation. mTORC1 specifically drives the eIF4E-mediated formation of SG through the phosphorylation of 4E-BP1, a key factor known to inhibit formation of the mTORC1-dependent eIF4E-eIF4GI interactions. Disrupting formation of SG by inactivation of mTOR with its specific inhibitor pp242 or by depletion of eIF4E or eIF4GI blocks the SG-associated antiapoptotic p21 pathway. Finally, pp242 sensitizes cancer cells to death in vitro and inhibits the growth of chemoresistant tumors in vivo. This work therefore highlights a novel role of the oncogenic mTORC1-eIF4E pathway, namely, the promotion of formation of antiapoptotic SG.
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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.