ArticleMolecular and cellular biology2003
Caveolin-1 maintains activated Akt in prostate cancer cells through scaffolding domain binding site interactions with and inhibition of serine/threonine protein phosphatases PP1 and PP2A.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
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Who cites it
124 citing papers in PubMed, 295 citations in OpenAlex.
- Cholesterol metabolism dysregulation in eyelid sebaceous gland carcinoma and its clinical significance.Indian journal of ophthalmology · 2026Article
- Screening anticancer peptides performance in organotypic prostate tumor-stroma 3D models.International journal of cancer · 2026Article
- CAVPENET Peptide Inhibits Prostate Cancer Cells Proliferation and Migration through PP1γ-Dependent Inhibition of AKT Signaling.Pharmaceutics · 2024Article
- Transepithelial transport of nanoparticles in oral drug delivery: From the perspective of surface and holistic property modulation.Acta pharmaceutica Sinica. B · 2024Review
- CRABP1-complexes in exosome secretion.Cell communication and signaling : CCS · 2024Article
- Cinobufagin disrupts the stability of lipid rafts by inhibiting the expression of caveolin-1 to promote non-small cell lung cancer cell apoptosis.Archives of medical science : AMS · 2024Article
- Caveolin-1-derived peptide attenuates cigarette smoke-induced airway and alveolar epithelial injury.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Molecular pathogenesis, mechanism and therapy of Cav1 in prostate cancer.Discover oncology · 2023Review
- PP1γ regulates neuronal insulin signaling and aggravates insulin resistance leading to AD-like phenotypes.Cell communication and signaling : CCS · 2023Article
- Mechanisms underlying divergent relationships between CaThe Journal of physiology · 2023Article
- Clustering analysis and prognostic model based on PI3K/AKT-related genes in pancreatic cancer.Frontiers in oncology · 2023Article
- Primary cilia and lipid raft dynamics.Open biology · 2021Review
- The Biomarker Potential of Caveolin-1 in Penile Cancer.Frontiers in oncology · 2021Article
- Posttranslational regulation of androgen dependent and independent androgen receptor activities in prostate cancer.Asian journal of urology · 2020Review
- Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer.Cancer metastasis reviews · 2020Review
- Deletion of caveolin scaffolding domain alters cancer cell migration.Cell cycle (Georgetown, Tex.) · 2019Article
- MIIP inhibits the growth of prostate cancer via interaction with PP1α and negative modulation of AKT signaling.Cell communication and signaling : CCS · 2019Article
- Prostate Cancer Energetics and Biosynthesis.Advances in experimental medicine and biology · 2019Review
- Akt-ing Up Just About Everywhere: Compartment-Specific Akt Activation and Function in Receptor Tyrosine Kinase Signaling.Frontiers in cell and developmental biology · 2019Review
- Protein Phosphatase 1 Regulatory Subunit SDS22 Inhibits Breast Cancer Cell Tumorigenesis by Functioning as a Negative Regulator of the AKT Signaling Pathway.Neoplasia (New York, N.Y.) · 2019Article
64 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previously it has been reported that caveolin-1 (cav-1) has antiapoptotic activities in prostate cancer cells and functions downstream of androgenic stimulation. In this study, we demonstrate that cav-1 overexpression significantly reduced thapsigargin (Tg)-stimulated apoptosis. Examination of the phosphatidylinositol 3-kinase (PI3-K)/Akt signaling cascade revealed higher activities of PDK1 and Akt but not PI3-K in cav-1-stimulated cells compared to control cells. We subsequently found that cav-1 interacts with and inhibits serine/threonine protein phosphatases PP1 and PP2A through scaffolding domain binding site interactions. Deletion of the cav-1 scaffolding domain significantly reduces phosphorylated Akt and cell viability compared with wild-type cav-1. Analysis of potential substrates for PP1 and PP2A revealed that cav-1-mediated inhibition of PP1 and PP2A leads to increased PDK1, Akt, and ERK1/2 activities. We demonstrate that increased Akt activities are largely responsible for cav-1-mediated cell survival using dominant-negative Akt mutants and specific inhibitors to MEK1/MEK and show that cav-1 increases the half-life of phosphorylated PDK1 and Akt after inhibition of PI3-K by LY294002. We further demonstrate that cav-1-stimulated Akt activities lead to increased phosphorylation of multiple Akt substrates, including GSK3, FKHR, and MDM2. In addition, overexpression of cav-1 significantly increases translocation of phosphorylated androgen receptor to nucleus. Our studies therefore reveal a novel mechanism of Akt activation in prostate cancer and potentially other malignancies.
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