ArticleJournal of cell science2016
Acid sphingomyelinase is required for cell surface presentation of Met receptor tyrosine kinase in cancer cells.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting VAMP5 suppresses PLK1-driven growth of gliomas with high NDRG4 expression.Journal of neuro-oncology · 2026Article
- Association of MET gene polymorphisms with breast cancer risk in Nigerian patients: a case-control study.BMC cancer · 2026Article
- SMPD1 as a Potential Prognostic Biomarker in Glioma Is Associated With an Immunosuppressive Microenvironment.CNS neuroscience & therapeutics · 2026Article
- Mir-16 Decreases the Expression of VTI1B and SMPD1, Genes Involved in Membrane-Protein Trafficking in Melanoma.Cancers · 2025Article
- Pancreatic Cancer Treatment Targeting the HGF/c-MET Pathway: The MEK Inhibitor Trametinib.Cancers · 2024Review
- Conditional knockdown of integrin beta-3 reveals its involvement in osteolytic and soft tissue lesions of breast cancer skeletal metastasis.Journal of cancer research and clinical oncology · 2021Article
- Proprotein convertase furin in SARS-CoV-2 and non-small cell lung cancer.Translational lung cancer research · 2020Article
- Syntaxin 6-mediated exosome secretion regulates enzalutamide resistance in prostate cancer.Molecular carcinogenesis · 2020Article
- Decreased Activity of Blood Acid Sphingomyelinase in the Course of Multiple Myeloma.International journal of molecular sciences · 2019Article
- Acid Sphingomyelinase regulates the localization and trafficking of palmitoylated proteins.Biology open · 2019Article
- N822K- or V560G-mutated KIT activation preferentially occurs in lipid rafts of the Golgi apparatus in leukemia cells.Cell communication and signaling : CCS · 2019Article
- Overexpression-mediated activation of MET in the Golgi promotes HER3/ERBB3 phosphorylation.Oncogene · 2019Article
- Induction of MET Receptor Tyrosine Kinase Down-regulation through Antibody-mediated Receptor Clustering.Scientific reports · 2019Article
- High-Affinity Human Anti-c-Met IgG Conjugated to Oxaliplatin as Targeted Chemotherapy for Hepatocellular Carcinoma.Frontiers in oncology · 2019Article
- HGF-induced formation of the MET-AXL-ELMO2-DOCK180 complex promotes RAC1 activation, receptor clustering, and cancer cell migration and invasion.The Journal of biological chemistry · 2018Article
- Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities.Molecular cancer · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Receptor tyrosine kinases (RTKs) are embedded in the lipid bilayer of the plasma membrane, but the specific roles of various lipids in cell signaling remain largely uncharacterized. We have previously found that acid sphingomyelinase (ASM; also known as SMPD1) regulates the conserved DAF-2 (the ortholog IGF-1R in mammals) RTK signaling pathway in Caenorhabditis elegans How ASM and its catalytic products, ceramides, control RTK signaling pathways remain unclear. Here, we report that ASM regulates the homeostasis of Met, an RTK that is frequently overexpressed in various cancers. Inactivation of ASM led to a rapid loss of Met from the plasma membrane, reduced Met phosphorylation and activation, and induced Met accumulation in the trans-Golgi network (TGN). However, trafficking of integrin β3 and vesicular stomatitis virus glycoprotein (VSVG) was largely unaffected. Knockdown of syntaxin 6 (STX6) also blocked the Golgi exit of Met. Depletion of either ASM or STX6 led to aberrant trafficking of Met to lysosomes, promoting its degradation. Our studies reveal that ASM and ceramides, together with STX6 and cholesterol, constitute a new regulatory mechanism for the exit of Met from the Golgi during its biosynthetic route, which is used to rapidly replenish and regulate the plasma membrane levels of Met in various cancer cells.
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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.