ArticleProceedings of the National Academy of Sciences of the United States of America2018
Role for ERK1/2-dependent activation of FCHSD2 in cancer cell-selective regulation of clathrin-mediated endocytosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 45 citations in OpenAlex.
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- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.bioRxiv : the preprint server for biology · 2025Article
- Novel kinase regulators of extracellular matrix internalisation identified by high-content screening modulate invasive carcinoma cell migration.PLoS biology · 2024Article
- Impact and Mechanisms of Action of BDNF on Neurological Disorders, Cancer, and Cardiovascular Diseases.CNS neuroscience & therapeutics · 2024Review
- Endosomal actin branching, fission, and receptor recycling require FCHSD2 recruitment by MICAL-L1.Molecular biology of the cell · 2024Article
- Inhibition of oxidative stress-induced epithelial-mesenchymal transition in retinal pigment epithelial cells of age-related macular degeneration model by suppressing ERK activation.Journal of advanced research · 2024Article
- Adaptations of membrane trafficking in cancer and tumorigenesis.Journal of cell science · 2024Review
- Tension-induced adhesion mode switching: the interplay between focal adhesions and clathrin-containing adhesion complexes.bioRxiv : the preprint server for biology · 2024Article
- Identification of a novel endocytosis‑associated gene signature for prognostic prediction in lung adenocarcinoma.Oncology letters · 2023Article
- PTPN23 ubiquitination by WDR4 suppresses EGFR and c-MET degradation to define a lung cancer therapeutic target.Cell death & disease · 2023Article
- The 'omics of obesity in B-cell acute lymphoblastic leukemia.Journal of the National Cancer Institute. Monographs · 2023Article
- Clathrin coats partially preassemble and subsequently bend during endocytosis.The Journal of cell biology · 2023Article
- Local regulation of extracellular vesicle traffic by the synaptic endocytic machinery.The Journal of cell biology · 2022Article
- Rapamycin inhibits oral cancer cell growth by promoting oxidative stress and suppressing ERK1/2, NF-κB and beta-catenin pathways.Frontiers in oncology · 2022Article
- Discovery of a dual Ras and ARF6 inhibitor from a GPCR endocytosis screen.Nature communications · 2021Article
- Article
- Loss of FCHSD1 leads to amelioration of chronic obstructive pulmonary disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Chromatin 3D interaction analysis of the STARD10 locus unveils FCHSD2 as a regulator of insulin secretion.Cell reports · 2021Article
- TNF-α signaling regulates RUNX1 function in endothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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3 authors at 1 institution in 1 country.
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Abstract
Clathrin-mediated endocytosis (CME) regulates the uptake of cell-surface receptors as well as their downstream signaling activities. We recently reported that signaling can reciprocally regulate CME in cancer cells and that this crosstalk can contribute to cancer progression. To further explore the nature and extent of the crosstalk between signaling and CME in cancer cell biology, we analyzed a panel of oncogenic signaling kinase inhibitors for their effects on CME across a panel of normal and cancerous cells. Inhibition of several kinases selectively affected CME in cancer cells, including inhibition of ERK1/2, which selectively inhibited CME by decreasing the rate of clathrin-coated pit (CCP) initiation. We identified an ERK1/2 substrate, the FCH/F-BAR and SH3 domain-containing protein FCHSD2, as being essential for the ERK1/2-dependent effects on CME and CCP initiation. Our data suggest that ERK1/2 phosphorylation activates FCHSD2 and regulates EGF receptor (EGFR) endocytic trafficking as well as downstream signaling activities. Loss of FCHSD2 activity in nonsmall cell lung cancer (NSCLC) cells leads to increased cell-surface expression and altered signaling downstream of EGFR, resulting in enhanced cell proliferation and migration. The expression level of FCHSD2 is positively correlated with higher NSCLC patient survival rates, suggesting that FCHSD2 can negatively affect cancer progression. These findings provide insight into the mechanisms and consequences of the reciprocal regulation of signaling and CME in cancer cells.
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