ArticleBritish journal of cancer2009
Activated 4E-BP1 represses tumourigenesis and IGF-I-mediated activation of the eIF4F complex in mesothelioma.
Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Biological functions and research progress of eIF4E.Frontiers in oncology · 2023Review
- 4Ei-10 interdiction of oncogenic cap-mediated translation as therapy for non-small cell lung cancer.Investigational new drugs · 2021Article
- Malignant pleural mesothelioma co-opts BCL-XCell death & disease · 2021Article
- Repression of oncogenic cap-mediated translation by 4Ei-10 diminishes proliferation, enhances chemosensitivity and alters expression of malignancy-related proteins in mesothelioma.Cancer chemotherapy and pharmacology · 2020Article
- Repression of oncogenic cap-mediated translation by 4Ei-10 diminishes proliferation, enhances chemosensitivity and alters expression of malignancy-related proteins in mesothelioma.Cancer chemotherapy and pharmacology · 2020Article
- Therapeutic Landscape of Malignant Pleural Mesothelioma: Collateral Vulnerabilities and Evolutionary Dependencies in the Spotlight.Frontiers in oncology · 2020Review
- Inhibition of oncogenic cap-dependent translation by 4EGI-1 reduces growth, enhances chemosensitivity and alters genome-wide translation in non-small cell lung cancer.Cancer gene therapy · 2019Article
- Cap-dependent translational control of oncolytic measles virus infection in malignant mesothelioma.Oncotarget · 2017Article
- Targeting eukaryotic protein translation in mesothelioma.Translational lung cancer research · 2017Review
- Si Shen Wan Regulates Phospholipase Cγ-1 and PI3K/Akt Signal in Colonic Mucosa from Rats with Colitis.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Nonamplified FGFR1 is a growth driver in malignant pleural mesothelioma.Molecular cancer research : MCR · 2014Article
- Small-molecule inhibition of oncogenic eukaryotic protein translation in mesothelioma cells.Investigational new drugs · 2014Article
- Multipoint targeting of the PI3K/mTOR pathway in mesothelioma.British journal of cancer · 2014Article
- Resistance to EGFR-TKI can be mediated through multiple signaling pathways converging upon cap-dependent translation in EGFR-wild type NSCLC.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2013Article
- Article
- Targeting eukaryotic translation in mesothelioma cells with an eIF4E-specific antisense oligonucleotide.PloS one · 2013Article
- Novel role of c-jun N-terminal kinase in regulating the initiation of cap-dependent translation.International journal of oncology · 2012Article
- Sensitivity of global translation to mTOR inhibition in REN cells depends on the equilibrium between eIF4E and 4E-BP1.PloS one · 2011Article
- Nuclear magnetic resonance in conjunction with functional genomics suggests mitochondrial dysfunction in a murine model of cancer cachexia.International journal of molecular medicine · 2011Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundInsulin-like growth factor (IGF)-I signalling stimulates proliferation, survival, and invasion in malignant mesothelioma and other tumour types. Studies have found that tumourigenesis is linked to dysregulation of cap-dependent protein translation.
methodsThe effect of IGF stimulation on cap-mediated translation activation in mesothelioma cell lines was studied using binding assays to a synthetic 7-methyl GTP-cap analogue. In addition, cap-mediated translation was genetically repressed in these cells with a dominant active motive of 4E-BP1.
resultsIn most mesothelioma cell lines, IGF-I stimulation resulted in a hyperphosphorylation-mediated inactivation of 4E-BP1 compared with that in normal mesothelial cells. An inhibitor of Akt diminished IGF-I-mediated phosphorylation of 4E-BP1, whereas inhibiting MAPK signalling had no such effect. IGF-I stimulation resulted in the activation of the cap-mediated translation complex as indicated by an increased eIF4G/eIF4E ratio in cap-affinity assays. Akt inhibition reversed the eIF4G/eIF4E ratio. Mesothelioma cells transfected with an activated 4E-BP1 protein (4E-BP1(A37/A46)) were resistant to IGF-I-mediated growth, motility, and colony formation. In a murine xenograft model, mesothelioma cells expressing the dominant active 4E-BP1(A37/A46) repressor protein showed abrogated tumourigenicity compared with control tumours.
conclusionIGF-I signalling in mesothelioma cells drives cell proliferation, motility, and tumourigenesis through its ability to activate cap-mediated protein translation complex through PI3K/Akt/mTOR signalling.
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