ArticleCancer science2013
Implication of 14-3-3ε and 14-3-3θ/τ in proteasome inhibition-induced apoptosis of glioma cells.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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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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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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- Recent advancements in tissue dissociation techniques for cell manufacturing single-cell analysis and downstream processing.Stem cells translational medicine · 2025Review
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- 14-3-3ε: a protein with complex physiology function but promising therapeutic potential in cancer.Cell communication and signaling : CCS · 2024Review
- Optimizing Phosphopeptide Structures That Target 14-3-3ε in Cutaneous Squamous Cell Carcinoma.ACS omega · 2024Article
- Optimizing Phosphopeptide Structures That Target 14-3-3ε in Cutaneous Squamous Cell Carcinoma.bioRxiv : the preprint server for biology · 2023Article
- Atypical activation of signaling downstream of inactivated Bcr-Abl mediates chemoresistance in chronic myeloid leukemia.Journal of cell communication and signaling · 2022Article
- Pathways to Parkinson's disease: a spotlight on 14-3-3 proteins.NPJ Parkinson's disease · 2021Review
- 14-3-3 Proteins Are on the Crossroads of Cancer, Aging, and Age-Related Neurodegenerative Disease.International journal of molecular sciences · 2019Review
- Shuttling SLC2A4RG is regulated by 14-3-3θ to modulate cell survival via caspase-3 and caspase-6 in human glioma.EBioMedicine · 2019Article
- 14-3-3β exerts glioma-promoting effects and is associated with malignant progression and poor prognosis in patients with glioma.Experimental and therapeutic medicine · 2018Article
- A non-aggressive, highly efficient, enzymatic method for dissociation of human brain-tumors and brain-tissues to viable single-cells.BMC neuroscience · 2016Article
- Overexpression of 14-3-3θ promotes tumor metastasis and indicates poor prognosis in breast carcinoma.Oncotarget · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteasome inhibitors represent a novel class of anticancer agents that are used in the treatment of hematologic malignancies and various solid tumors. However, mechanisms underlying their anticancer actions were not fully understood. It has been reported that strong 14-3-3 protein expression is observed and associated with tumor genesis and progression of astrocytoma. In addition, global inhibition of 14-3-3 functions with a general 14-3-3 antagonist difopein induces apoptosis of human astrocytoma cells, validating 14-3-3 as a potential molecular target for anticancer therapeutic management. In the current study, for the first time we demonstrated that proteasome inhibitors downregulated 14-3-3ε and 14-3-3θ/τ in U87 and SF295 glioma cells. Overexpression of 14-3-3ε and 14-3-3θ/τ significantly suppressed apoptosis of human glioma cells induced by proteasome inhibitors. We also demonstrated that MG132 activated ASK1 and siASK1 compromised the MG132-induced apoptosis of glioma cells. Furthermore, overexpression of 14-3-3ε and 14-3-3θ/τ markedly suppressed activation of ASK1. Collectively, the current study supported that proteasome inhibitors, at least in part, caused cytotoxicity of glioma cells via downregulation of 14-3-3ε and 14-3-3θ/τ and subsequent activation of ASK1.
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What Socratic holds
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.