ArticleBlood2005
p130Cas mediates the transforming properties of the anaplastic lymphoma kinase.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 84 citations in OpenAlex.
- ALK fusion promotes metabolic reprogramming of cancer cells by transcriptionally upregulating PFKFB3.Oncogene · 2022Article
- Tyrosine phosphatases regulate resistance to ALK inhibitors in ALK+ anaplastic large cell lymphoma.Blood · 2022Article
- Novel germline mutation in lung cancer pedigrees establishesAnnals of translational medicine · 2022Article
- F-circEA1 regulates cell proliferation and apoptosis through ALK downstream signaling pathway in non-small cell lung cancer.Human cell · 2022Article
- NPM-ALK-Induced Reprogramming of Mature TCR-Stimulated T Cells Results in Dedifferentiation and Malignant Transformation.Cancer research · 2021Article
- Cytoskeleton Dynamics in Peripheral T Cell Lymphomas: An Intricate Network Sustaining Lymphomagenesis.Frontiers in oncology · 2021Review
- ALK phosphorylates SMAD4 on tyrosine to disable TGF-β tumour suppressor functions.Nature cell biology · 2019Article
- Anaplastic Lymphoma Kinase in Cutaneous Malignancies.Cancers · 2017Review
- NPM-ALK phosphorylates WASp Y102 and contributes to oncogenesis of anaplastic large cell lymphoma.Oncogene · 2017Article
- Coupling an EML4-ALK-centric interactome with RNA interference identifies sensitizers to ALK inhibitors.Science signaling · 2016Article
- Oncogenic ALK regulates EMT in non-small cell lung carcinoma through repression of the epithelial splicing regulatory protein 1.Oncotarget · 2016Article
- Oncogenic role of miR-155 in anaplastic large cell lymphoma lacking the t(2;5) translocation.The Journal of pathology · 2015Article
- Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology.Nature reviews. Cancer · 2013Review
- p130Cas/Cyclooxygenase-2 axis in the control of mesenchymal plasticity of breast cancer cells.Breast cancer research : BCR · 2012Article
- NSP-CAS Protein Complexes: Emerging Signaling Modules in Cancer.Genes & cancer · 2012Article
- Cas and NEDD9 Contribute to Tumor Progression through Dynamic Regulation of the Cytoskeleton.Genes & cancer · 2012Article
- Silencing of p130cas in ovarian carcinoma: a novel mechanism for tumor cell death.Journal of the National Cancer Institute · 2011Article
- Fusion tyrosine kinase NPM-ALK Deregulates MSH2 and suppresses DNA mismatch repair function novel insights into a potent oncoprotein.The American journal of pathology · 2011Article
- Inhibition of Rac controls NPM-ALK-dependent lymphoma development and dissemination.Blood cancer journal · 2011Article
- Research progresses in the pathogenesis of anaplastic large cell lymphoma.Chinese journal of cancer · 2011Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Translocations of the anaplastic lymphoma kinase (ALK) gene have been described in anaplastic large-cell lymphomas (ALCLs) and in stromal tumors. The most frequent translocation, t(2;5), generates the fusion protein nucleophosmin (NPM)-ALK with intrinsic tyrosine kinase activity. Along with transformation, NPM-ALK induces morphologic changes in fibroblasts and lymphoid cells, suggesting a direct role of ALK in cell shaping. In this study, we used a mass-spectrometry-based proteomic approach to search for proteins involved in cytoskeleton remodeling and identified p130Cas (p130 Crk-associated substrate) as a novel interactor of NPM-ALK. In 293 cells and in fibroblasts as well as in human ALK-positive lymphoma cell lines, NPM-ALK was able to bind p130Cas and to induce its phosphorylation. Both of the effects were dependent on ALK kinase activity and on the adaptor protein growth factor receptor-bound protein 2 (Grb2), since no binding or phosphorylation was found with the kinase-dead mutant NPM-ALK(K210R) or in the presence of a Grb2 dominant-negative protein. Phosphorylation of p130Cas by NPM-ALK was partially independent from Src (tyrosine kinase pp60c-src) kinase activity, as it was still detectable in Syf-/- cells. Finally, p130Cas-/- (also known as Bcar1-/-) fibroblasts expressing NPM-ALK showed impaired actin filament depolymerization and were no longer transformed compared with wild-type cells, indicating an essential role of p130Cas activation in ALK-mediated transformation.
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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.