ArticleOncotarget2016
The Hippo transducer TAZ promotes cell proliferation and tumor formation of glioblastoma cells through EGFR pathway.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Disrupted Signalling Landscapes in Glioblastoma: Mechanistic Insights and Therapeutic Frontiers.Biology · 2026Review
- Metabolic remodeling and immune evasion in glioblastoma: a focus on serine and lipid networks.Frontiers in oncology · 2026Review
- Modelling quiescence exit of neural stem cells reveals a FOXG1-FOXO6 axis.Disease models & mechanisms · 2024Article
- Anti-invasive efficacy and survival benefit of the YAP-TEAD inhibitor verteporfin in preclinical glioblastoma models.Neuro-oncology · 2022Article
- The Hippo pathway effectors YAP and TAZ interact with EGF-like signaling to regulate expansion-related events in bovine cumulus cells in vitro.Journal of assisted reproduction and genetics · 2022Article
- Review
- EGFR Activates a TAZ-Driven Oncogenic Program in Glioblastoma.Cancer research · 2021Article
- Hippo Signaling Pathway in Gliomas.Cells · 2021Review
- Article
- Yap haploinsufficiency leads to Müller cell dysfunction and late-onset cone dystrophy.Cell death & disease · 2020Article
- Harnessing the Potential Synergistic Interplay Between Photosensitizer Dark Toxicity and Chemotherapy.Photochemistry and photobiology · 2020Article
- Autocrine CXCL8-dependent invasiveness triggers modulation of actin cytoskeletal network and cell dynamics.Aging · 2020Article
- Proton Therapy and Src Family Kinase Inhibitor Combined Treatments on U87 Human Glioblastoma Multiforme Cell Line.International journal of molecular sciences · 2019Article
- TP53BP2 decreases cell proliferation and induces autophagy in neuroblastoma cell lines.Oncology letters · 2019Article
- miR-125a-5p inhibits colorectal cancer cell epithelial-mesenchymal transition, invasion and migration by targeting TAZ.OncoTargets and therapy · 2019Article
- IRS-1 increases TAZ expression and promotes osteogenic differentiation in rat bone marrow mesenchymal stem cells.Biology open · 2018Article
- Ars2 promotes cell proliferation and tumorigenicity in glioblastoma through regulating miR-6798-3p.Scientific reports · 2018Article
- Analysis of chromatin accessibility uncovers TEAD1 as a regulator of migration in human glioblastoma.Nature communications · 2018Article
- MicroRNA-137 inhibits growth of glioblastoma through EGFR suppression.American journal of translational research · 2017Article
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
No grant is acknowledged in the PubMed record.
Abstract
TAZ, a WW-domain-containing transcriptional co-activator, is important for development of various tissues in mammals. Recently, TAZ has been found to be overexpressed in some types of human cancers. However, the role of TAZ in glioblastoma remains unclear. In this study, we found that TAZ was overexpressed in prognostically poor glioblastoma patients. Through knocking down or overexpressing TAZ in U87 and LN229 cells, the expression level of TAZ was found to be positively related to cell proliferation in vitro and tumor formation in vivo. Further investigation indicated that TAZ could significantly promote the acceleration of cell cycle. Moreover, the western blot for p-EGFR, p-AKT, p-ERK1/2, p21, cyclin E and CDK2 proteins, target genes of the EGFR pathway, indicated that TAZ significantly activated EGFR/AKT/ERK signaling. Additionally, the blockage of EGFR pathway resulted in a significantly inhibition of cell proliferation induced by TAZ. Taken together, these results demonstrate that TAZ can promote proliferation and tumor formation in glioblastoma cells by potentiating the EGFR/AKT/ERK pathway, and provide the evidence for promising target for the treatment of glioblastoma.
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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 OpenQuestion graph.