ArticleOncology letters2017
Transcriptional co-activator with PDZ-binding motif overexpression promotes cell proliferation and transcriptional co-activator with PDZ-binding motif deficiency induces cell cycle arrest in neuroblastoma.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Review
- Review
- A New Player in Neuroblastoma: YAP and Its Role in the Neuroblastoma Microenvironment.Cancers · 2021Review
- CDGSH Iron Sulfur Domain 2 Deficiency Inhibits Cell Proliferation and Induces Cell Differentiation of Neuroblastoma.Pathology oncology research : POR · 2020Article
- TP53BP2 decreases cell proliferation and induces autophagy in neuroblastoma cell lines.Oncology letters · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional co-activator with PDZ-binding motif (TAZ) is a transcriptional co-activator which binds to a variety of transcription factors. An increasing number of studies have provided evidence that TAZ may be a positive regulator of cell proliferation and tumorigenesis. To reveal the underlying mechanisms by which TAZ controls these cellular processes, the present study used lentivirus expression system, flow cytometry, immunofluorescence and subcutaneous xenograft assays. The present study demonstrated that TAZ promoted and was indispensable for neuroblastoma cell proliferation and tumorigenesis. Additional mechanistic assays revealed that the downregulation of TAZ induced cell cycle arrest in the G1 phase, which may be mediated through the inhibition of cyclin E2 expression. These findings indicated that TAZ may serve as a potential neuroblastoma therapeutic target.
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Registered trials
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