ArticlePloS one2014
Opposing effects of PI3K/Akt and Smad-dependent signaling pathways in NAG-1-induced glioblastoma cell apoptosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 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
16 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- The purple mangosteen (Garcinia mangostana): Defining the anticancer potential of selected xanthones.Pharmacological research · 2022Review
- GDF15 expression in glioma is associated with malignant progression, immune microenvironment, and serves as a prognostic factor.CNS neuroscience & therapeutics · 2022Article
- GDF15, an update of the physiological and pathological roles it plays: a review.Pflugers Archiv : European journal of physiology · 2020Review
- The Role of Growth Differentiation Factor 15 in Energy Metabolism.Diabetes & metabolism journal · 2020Review
- Analysis and Simulation of Glioblastoma Cell Lines-Derived Extracellular Vesicles Metabolome.Metabolites · 2020Article
- Growth differentiation factor 15 (GDF15): A survival protein with therapeutic potential in metabolic diseases.Pharmacology & therapeutics · 2019Review
- Mechanical Compression Regulates Brain Cancer Cell Migration Through MEK1/Erk1 Pathway Activation and GDF15 Expression.Frontiers in oncology · 2019Article
- Distinct response to GDF15 knockdown in pediatric and adult glioblastoma cell lines.Journal of neuro-oncology · 2018Article
- Dexamethasone induced apoptosis of A549 cells via the TGF-β1/Smad2 pathway.Oncology letters · 2018Article
- Review
- Correction: Opposing Effects of PI3K/Akt and Smad-Dependent Signaling Pathways in NAG-1-Induced Glioblastoma Cell Apoptosis.PloS one · 2018Article
- NF-κB regulates GDF-15 to suppress macrophage surveillance during early tumor development.The Journal of clinical investigation · 2017Article
- Growth Differentiation Factor 15 Is Associated With Major Amputation and Mortality in Patients With Peripheral Artery Disease.Journal of the American Heart Association · 2017Article
- MicroRNA-564 is downregulated in glioblastoma and inhibited proliferation and invasion of glioblastoma cells by targeting TGF-β1.Oncotarget · 2016Article
- PCAF-mediated Akt1 acetylation enhances the proliferation of human glioblastoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonsteroidal anti-inflammatory drug (NSAID) activated gene-1 (NAG-1) is a divergent member of the transforming growth factor-beta (TGF-β) superfamily. NAG-1 plays remarkable multifunctional roles in controlling diverse physiological and pathological processes including cancer. Like other TGF-β family members, NAG-1 can play dual roles during cancer development and progression by negatively or positively modulating cancer cell behaviors. In glioblastoma brain tumors, NAG-1 appears to act as a tumor suppressor gene; however, the precise underlying mechanisms have not been well elucidated. In the present study, we discovered that overexpression of NAG-1 induced apoptosis in U87 MG, U118 MG, U251 MG, and T98G cell lines via the intrinsic mitochondrial pathway, but not in A172 and LN-229 cell lines. NAG-1 could induce the phosphorylation of PI3K/Akt and Smad2/3 in all six tested glioblastoma cell lines, except Smad3 phosphorylation in A172 and LN-229 cell lines. In fact, Smad3 expression and its phosphorylation were almost undetectable in A172 and LN-229 cells. The PI3K inhibitors promoted NAG-1-induced glioblastoma cell apoptosis, while siRNAs to Smad2 and Smad3 decreased the apoptosis rate. NAG-1 also stimulated the direct interaction between Akt and Smad3 in glioblastoma cells. Elevating the level of Smad3 restored the sensitivity to NAG-1-induced apoptosis in A172 and LN-229 cells. In conclusion, our results suggest that PI3K/Akt and Smad-dependent signaling pathways display opposing effects in NAG-1-induced glioblastoma cell apoptosis.
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.