ArticleOncogene2012
Overexpression of 14-3-3ζ in cancer cells activates PI3K via binding the p85 regulatory subunit.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
58 citing papers in PubMed, 97 citations in OpenAlex.
- YWHAG overexpression correlates with an immune-desert microenvironment and poor prognosis in laryngeal squamous cell carcinoma.Frontiers in immunology · 2026Article
- The Interaction between miRNAs and 14-3-3ζ Protein in Different Diseases.Protein and peptide letters · 2025Review
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- Review
- TargetingHeliyon · 2024Article
- Ezetimibe Lowers Risk of Alzheimer's and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction.Aging biology · 2024Article
- 14-3-3η Proteins as a Diagnostic Marker, Disease Activation Indicator, and Lymphoma Predictor in Patients with Primary Sjögren Syndrome.Archives of Iranian medicine · 2023Article
- YBX1 regulates the survival of chronic myeloid leukemia stem cells by modulating mCellular oncology (Dordrecht, Netherlands) · 2023Article
- Impact of Sacubitril/Valsartan on Circulating microRNA in Patients with Heart Failure.Biomedicines · 2023Article
- High-Resolution Crystal Structure of Muscle Phosphoglycerate Mutase Provides Insight into Its Nuclear Import and Role.International journal of molecular sciences · 2022Article
- miR-29b-3p inhibits 22Rv1 prostate cancer cell proliferation through the YWHAE/BCL-2 regulatory axis.Oncology letters · 2022Article
- Review
- Downregulation of miR-128 Ameliorates Ang II-Induced Cardiac Remodeling via SIRT1/PIK3R1 Multiple Targets.Oxidative medicine and cellular longevity · 2021Article
- IGF2BP1, a Conserved Regulator of RNA Turnover in Cancer.Frontiers in molecular biosciences · 2021Article
- MiRNA-1225 Inhibits Osteosarcoma Tumor Growth and Progression by Targeting YWHAZ.OncoTargets and therapy · 2021Article
- Probing the 14-3-3 Isoform-Specificity Profile of Protein-Protein Interactions Stabilized by Fusicoccin A.ACS omega · 2020Article
- Article
- Down-regulation of 14-3-3zeta reduces proliferation and increases apoptosis in human glioblastoma.Cancer gene therapy · 2020Article
- Smad4 induces cell death in HO-8910 and SKOV3 ovarian carcinoma cell lines via PI3K-mTOR involvement.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Matrix regeneration proteins in the hypoxia-triggered exosomes of shoulder tenocytes and adipose-derived mesenchymal stem cells.Molecular and cellular biochemistry · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The ubiquitously expressed 14-3-3 proteins regulate many pathways involved in transformation. Previously, we found that 14-3-3ζ overexpression increased Akt phosphorylation in human mammary epithelial cells. Here, we investigated the clinical relevance and molecular mechanism of 14-3-3ζ-overexpression-mediated Akt phosphorylation, and its potential impact on breast cancer progression. We found that 14-3-3ζ overexpression was significantly (P=0.005) associated with increased Akt phosphorylation in human breast tumors. Additionally, 14-3-3ζ overexpression combined with strong Akt phosphorylation was significantly (P=0.01) associated with increased cancer recurrence in patients. In contrast, knockdown of 14-3-3ζ expression by small interfering RNA in cancer cell lines and tumor xenografts reduced Akt phosphorylation. Furthermore, 14-3-3ζ enhanced Akt phosphorylation through activation of phosphoinositide 3-kinase (PI3K). Mechanistically, 14-3-3ζ bound to the p85 regulatory subunit of PI3K and increased PI3K translocation to the cell membrane. A single 14-3-3-binding motif encompassing serine 83 on p85 is largely responsible for 14-3-3ζ-mediated p85 binding and PI3K/Akt activation. Mutation of serine 83 to alanine on p85 inhibited 14-3-3ζ binding to the p85 subunit of PI3K, reduced PI3K membrane localization and activation, impeded anchorage-independent growth and enhanced stress-induced apoptosis. These findings revealed a novel mechanism by which 14-3-3ζ overexpression activates PI3K, a key node in the mitogenic signaling network known to promote malignancies in many cell types.
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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 Socratic graph.