ArticleMolecular neurobiology2018
14-3-3β Depletion Drives a Senescence Program in Glioblastoma Cells Through the ERK/SKP2/p27 Pathway.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- SKping cell cycle regulation: role of ubiquitin ligase SKP2 in hematological malignancies.Frontiers in oncology · 2024Review
- Inducible Knockout of 14-3-3β Attenuates Proliferation and Spheroid Formation in a Human Glioblastoma Cell Line U87MG.Brain sciences · 2023Article
- Small-molecule compounds inhibiting S-phase kinase-associated protein 2: A review.Frontiers in pharmacology · 2023Review
- 14-3-3β is essential for milk composition stimulated by Leu/IGF-1 via IGF1R signaling pathway in BMECs.In vitro cellular & developmental biology. Animal · 2022Article
- Hypoxia Promotes Glioma Stem Cell Proliferation by Enhancing the 14-3-3Journal of immunology research · 2022Article
- CAMSAP3 depletion induces lung cancer cell senescence-associated phenotypes through extracellular signal-regulated kinase inactivation.Cancer medicine · 2021Article
- Hexokinase 2 Promotes Cell Growth and Tumor Formation Through the Raf/MEK/ERK Signaling Pathway in Cervical Cancer.Frontiers in oncology · 2020Article
- Glioblastoma chemoresistance: roles of the mitochondrial melatonergic pathway.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- Adaptor protein LNK promotes anaplastic thyroid carcinoma cell growth via 14-3-3 ε/γ binding.Cancer cell international · 2020Article
- MiR-129-5p sensitization of lung cancer cells to etoposide-induced apoptosis by reducing YWHAB.Journal of Cancer · 2020Article
- 14-3-3ζ targeting induced senescence in Hep-2 laryngeal cancer cell through deneddylation of Cullin1 in the Skp1-Cullin-F-box protein complex.Cell proliferation · 2019Article
- 14-3-3 Proteins Are on the Crossroads of Cancer, Aging, and Age-Related Neurodegenerative Disease.International journal of molecular sciences · 2019Review
- Low Expression of 14-3-3beta Is Associated With Adverse Survival of Diffuse Large B-Cell Lymphoma Patients.Frontiers in medicine · 2019Article
- An Interplay between Senescence, Apoptosis and Autophagy in Glioblastoma Multiforme-Role in Pathogenesis and Therapeutic Perspective.International journal of molecular sciences · 2018Review
- Inhibition of H3K27me3 Histone Demethylase Activity Prevents the Proliferative Regeneration of Zebrafish Lateral Line Neuromasts.Frontiers in molecular neuroscience · 2017Article
- Combination Treatment with PPARBioMed research international · 2017Article
- KRIBB11 Exerts Anticancer Effects on A172 Glioblastoma CellsCancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The induction of senescence in cancer cells has recently been implicated as a mechanism of tumor regression in response to various modes of stress. 14-3-3 proteins are conserved scaffolding molecules that are involved in various cellular functions. Among the seven isoforms, 14-3-3β is specifically expressed in astrocytoma in correlation with the malignancy grade. We investigated the possible role of 14-3-3β in the regulation of senescence induction in A172 glioblastoma cells. The knockdown of 14-3-3β by specific small interfering RNA resulted in a significant change in cellular phenotypes and an increase in cells staining positive for senescence-associated β-galactosidase. Western blotting of the 14-3-3β-depleted A172 cells revealed increased p27 expression and decreased SKP2 expression, while the expression of p53 and p21 was not altered. Subsequently, we demonstrated that ERK is a key modulator of SKP2/p27 axis activity in 14-3-3β-mediated senescence based on the following: (1) 14-3-3β knockdown decreased p-ERK levels; (2) treatment with U0126, an MEK inhibitor, completely reproduced the senescence morphology as well as the expression profiles of p27 and SKP2; and (3) the senescence phenotypes induced by 14-3-3β depletion were considerably recovered by constitutively active ERK expression. Our results indicate that 14-3-3β negatively regulates senescence in glioblastoma cells via the ERK/SKP2/p27 pathway. Furthermore, 14-3-3β depletion also resulted in senescence phenotypes in U87 glioblastoma cells, suggesting that 14-3-3β could be targeted to induce premature senescence as a therapeutic strategy against glioblastoma progression.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.