ArticleMolecular and cellular biology2006
The insulin-like growth factor I receptor is required for Akt activation and suppression of anoikis in cells transformed by the ETV6-NTRK3 chimeric tyrosine kinase.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 73 citations in OpenAlex.
- Methods for Identifying Patients with Tropomyosin Receptor Kinase (TRK) Fusion Cancer.Pathology oncology research : POR · 2020Review
- Review
- SHOC2 phosphatase-dependent RAF dimerization mediates resistance to MEK inhibition in RAS-mutant cancers.Nature communications · 2019Article
- Insulin-like growth factor 1 receptor stabilizes the ETV6-NTRK3 chimeric oncoprotein by blocking its KPC1/Rnf123-mediated proteasomal degradation.The Journal of biological chemistry · 2018Article
- Loss of PRP4K drives anoikis resistance in part by dysregulation of epidermal growth factor receptor endosomal trafficking.Oncogene · 2018Article
- Detecting and targetting oncogenic fusion proteins in the genomic era.Biology of the cell · 2015Review
- Can we unlock the potential of IGF-1R inhibition in cancer therapy?Cancer treatment reviews · 2014Review
- Cancer cell survival during detachment from the ECM: multiple barriers to tumour progression.Nature reviews. Cancer · 2014Review
- Inhibition of c-Src blocks oestrogen-induced apoptosis and restores oestrogen-stimulated growth in long-term oestrogen-deprived breast cancer cells.European journal of cancer (Oxford, England : 1990) · 2014Article
- Identification of kinase fusion oncogenes in post-Chernobyl radiation-induced thyroid cancers.The Journal of clinical investigation · 2013Article
- Mutation of the salt bridge-forming residues in the ETV6-SAM domain interface blocks ETV6-NTRK3-induced cellular transformation.The Journal of biological chemistry · 2013Article
- Mechanisms that link the oncogenic epithelial-mesenchymal transition to suppression of anoikis.Journal of cell science · 2013Review
- Targeting the insulin growth factor receptor 1.Hematology/oncology clinics of North America · 2012Review
- Metformin accelerates the growth of BRAF V600E-driven melanoma by upregulating VEGF-A.Cancer discovery · 2012Article
- Article
- The AMPK stress response pathway mediates anoikis resistance through inhibition of mTOR and suppression of protein synthesis.Cell death and differentiation · 2012Article
- Inhibition of PI3K/mTOR leads to adaptive resistance in matrix-attached cancer cells.Cancer cell · 2012Article
- Article
- MMP13 mediates cell cycle progression in melanocytes and melanoma cells: in vitro studies of migration and proliferation.Molecular cancer · 2010Article
- PTK6 regulates IGF-1-induced anchorage-independent survival.PloS one · 2010Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signaling through the insulin-like growth factor I receptor (IGF-IR) axis is essential for transformation by many dominantly acting oncoproteins. However, the mechanism by which IGF-IR contributes to oncogenesis remains unknown. To examine this, we compared transformation properties of the oncogenic ETV6-NTRK3 (EN) chimeric tyrosine kinase in IGF-IR-null R- mouse embryo fibroblasts with R- cells engineered to reexpress IGF-IR (R+ cells). We previously showed that R- cells expressing EN (R- EN cells) are resistant to transformation but that transformation is restored in R+ cells. We now show that while R- EN cells have intact Ras-extracellular signal-regulated kinase signaling and cell cycle progression, they are defective in phosphatidylinositol-3-kinase (PI3K)-Akt activation and undergo detachment-induced apoptosis (anoikis) under anchorage-independent conditions. In contrast, R+ cells expressing EN (R+ EN cells) suppress anoikis and are fully transformed. The requirement for IGF-IR in R- EN cells is overcome by ectopic expression of either activated Akt or a membrane-targeted form of EN. Moreover, compared to R- EN cells, R+ EN cells show a dramatic increase in membrane localization of insulin receptor substrate 1 (IRS-1) in association with EN. Since EN is known to bind IRS-1 as an adaptor protein, our findings suggest that IGF-IR may function to localize EN/IRS-1 complexes to cell membranes, in turn facilitating PI3K-Akt activation and suppression of anoikis.
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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 Socratic graph.