ArticleNeoplasia (New York, N.Y.)
Degradation and dephosphorylation of focal adhesion kinase during okadaic acid-induced apoptosis in human neuroblastoma cells.
Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Sea Squirt-Derived Peptide WLP Mitigates OKA-Induced Alzheimer's Disease-like Phenotypes in Human Cerebral Organoid.Antioxidants (Basel, Switzerland) · 2025Article
- Gefitinib induces anoikis in cervical cancer cells.BMB reports · 2024Article
- Article
- Epithelial cell extrusion: Pathways and pathologies.Seminars in cell & developmental biology · 2017Review
- Cbl-b promotes cell detachment via ubiquitination of focal adhesion kinase.Oncology letters · 2016Article
- Identification of dynamic changes in proteins associated with the cellular cytoskeleton after exposure to okadaic acid.Marine drugs · 2013Article
- Triptolide-Mediated Apoptosis by Suppression of Focal Adhesion Kinase through Extrinsic and Intrinsic Pathways in Human Melanoma Cells.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Identification of subtilase cytotoxin (SubAB) receptors whose signaling, in association with SubAB-induced BiP cleavage, is responsible for apoptosis in HeLa cells.Infection and immunity · 2011Article
- MYCN, neuroblastoma and focal adhesion kinase (FAK).Frontiers in bioscience (Elite edition) · 2011Review
- Focal adhesion kinase as a cancer therapy target.Anti-cancer agents in medicinal chemistry · 2010Review
- Targeting focal adhesion kinase in neuroblastoma.Anti-cancer agents in medicinal chemistry · 2010Review
- HO-3867, a synthetic compound, inhibits the migration and invasion of ovarian carcinoma cells through downregulation of fatty acid synthase and focal adhesion kinase.Molecular cancer research : MCR · 2010Article
- Inhibition of focal adhesion kinase decreases tumor growth in human neuroblastoma.Cell cycle (Georgetown, Tex.) · 2010Article
- Inhibition of focal adhesion kinase and src increases detachment and apoptosis in human neuroblastoma cell lines.Molecular carcinogenesis · 2010Article
- The methyl ester of okadaic acid is more potent than okadaic acid in disrupting the actin cytoskeleton and metabolism of primary cultured hepatocytes.British journal of pharmacology · 2010Article
- Insulin receptor substrate (IRS)-2, not IRS-1, protects human neuroblastoma cells against apoptosis.Apoptosis : an international journal on programmed cell death · 2009Article
- A review of the past, present, and future directions of neoplasia.Neoplasia (New York, N.Y.) · 2005Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Focal adhesion kinase (FAK) prevents apoptosis in many cell types. We have reported that tyrosine residues in FAK are dephosphorylated and FAK is degraded during mannitol-induced apoptosis in human neuroblastoma cells. Several studies suggest that FAK dephosphorylation and degradation are separate events. The current study defines the relationship between FAK dephosphorylation and degradation in neuroblastoma cells using okadaic acid (OA). OA, a serine phosphatase inhibitor, promotes serine/threonine phosphorylation, which in turn blocks tyrosine phosphorylation. OA induced focal adhesion loss, actin cytoskeleton disorganization, and cellular detachment, which corresponded to a loss of FAK Tyr397 phosphorylation. These changes preceded caspase-3 activation, Akt and MAP kinase activity loss, protein ubiquitination, and cellular apoptosis. Insulin-like growth factor-I prevented mannitol-induced, but not OA-induced, substrate detachment and FAK Tyr397 dephosphorylation, and the effects of OA on FAK Tyr397 phosphorylation were irreversible. The proteolytic degradation of FAK is temporally distinct from its tyrosine dephosphorylation, occurring when apoptotic pathways are already initiated and during a generalized destruction of signaling proteins. Therefore, agents resulting in the dephosphorylation of FAK may be beneficial for therapeutic treatment, irrespective of FAK protein levels, as this may result in apoptosis, which cannot be prevented by growth factor signaling.
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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.