ArticleThe FEBS journal2013
Phosphoproteomic analysis of anaplastic lymphoma kinase (ALK) downstream signaling pathways identifies signal transducer and activator of transcription 3 as a functional target of activated ALK in neuroblastoma cells.
Article in The FEBS journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- A structure-based virtual screening approach to identify novel anaplastic lymphoma kinase inhibitors.Journal of molecular modeling · 2026Article
- Rab3B Proteins: Cellular Functions, Regulatory Mechanisms, and Potential as a Cancer Therapy Target.Cell biochemistry and biophysics · 2025Review
- Anaplastic Lymphoma Kinase signaling stabilizes SLC3A2 expression via MARCH11 to promote neuroblastoma cell growth.Cell death and differentiation · 2024Article
- N-MYC impairs innate immune signaling in high-grade serous ovarian carcinoma.Science advances · 2024Article
- Metabolic protein kinase signalling in neuroblastoma.Molecular metabolism · 2023Review
- ALK fusion NSCLC oncogenes promote survival and inhibit NK cell responses viaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Gene utility recapitulates chromosomal aberrancies in advanced stage neuroblastoma.Computational and structural biotechnology journal · 2022Article
- Sustained Response to Entrectinib in an Infant With a Germline ALKAL2 Variant and Refractory Metastatic Neuroblastoma With Chromosomal 2p Gain and Anaplastic Lymphoma Kinase and Tropomyosin Receptor Kinase Activation.JCO precision oncology · 2022Article
- Defining Pathological Activities of ALK in Neuroblastoma, a Neural Crest-Derived Cancer.International journal of molecular sciences · 2021Review
- A highly multiplexed quantitative phosphosite assay for biology and preclinical studies.Molecular systems biology · 2021Article
- Identification of the Wallenda JNKKK as an Alk suppressor reveals increased competitiveness of Alk-expressing cells.Scientific reports · 2020Article
- Anaplastic Lymphoma Kinase Regulates Internalization of the Dopamine D2 Receptor.Molecular pharmacology · 2020Article
- Non-Genomic Control of DynamicFrontiers in oncology · 2020Review
- Preparation of a phosphotyrosine-protein standard for use in semiquantitative western blotting with enhanced chemiluminescence.PloS one · 2020Article
- Proteomic Phosphosite Analysis Identified Crucial NPM-ALK-Mediated NIPA Serine and Threonine Residues.International journal of molecular sciences · 2019Article
- Dual-Specificity Phosphatases in Neuroblastoma Cell Growth and Differentiation.International journal of molecular sciences · 2019Review
- A kinome-wide RNAi screen identifies ALK as a target to sensitize neuroblastoma cells for HDAC8-inhibitor treatment.Cell death and differentiation · 2018Article
- Clinical response of the novel activating ALK-I1171T mutation in neuroblastoma to the ALK inhibitor ceritinib.Cold Spring Harbor molecular case studies · 2018Article
- The ALK receptor in sympathetic neuron development and neuroblastoma.Cell and tissue research · 2018Review
- Review
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Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the anaplastic lymphoma kinase (ALK) receptor tyrosine kinase is a key oncogenic mechanism in a growing number of tumor types. In the majority of cases, ALK is activated by fusion with a dimerizing partner protein as a result of chromosomal translocation events, most studied in the case of the nucleophosmin-ALK and echinoderm microtubule-associated protein-like 4-ALK oncoproteins. It is now also appreciated that the full-length ALK receptor can be activated by point mutations and by deletions within the extracellular domain, such as those observed in neuroblastoma. Several studies have employed phosphoproteomics approaches to find substrates of ALK fusion proteins. In this study, we used MS-based phosphotyrosine profiling to characterize phosphotyrosine signaling events associated with the full-length ALK receptor. A number of previously identified and novel targets were identified. One of these, signal transducer and activator of transcription 3 (STAT3), has previously been observed to be activated in response to oncogenic ALK signaling, but the significance of this in signaling from the full-length ALK receptor has not been explored further. We show here that activated ALK robustly activates STAT3 on Tyr705 in a number of independent neuroblastoma cell lines. Furthermore, knockdown of STAT3 by RNA interference resulted in a reduction in myelocytomatosis neuroblastom (MYCN) protein levels downstream of ALK signaling. These observations, together with a decreased level of MYCN and inhibition of neuroblastoma cell growth in the presence of STAT3 inhibitors, suggest that activation of STAT3 is important for ALK signaling activity in neuroblastoma.
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