ArticleOncotarget2017
GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- The MYBL2-GTSE1 axis promotes laryngeal squamous cell carcinoma progression by regulating PI3K/AKT-dependent glycolytic reprogramming.Cancer biology & therapy · 2026Article
- 45A ncRNA Expression Leads to Chromosomal Instability and Cytoskeletal Dynamics Impairment by Modulating GTSE1/p53/AurB Subcellular Localization.International journal of molecular sciences · 2026Article
- Roles of TEAD Transcription Factors and their Coactivators in the Progression and Metastasis of Cancers.Recent patents on anti-cancer drug discovery · 2026Review
- Pan cancer characterization of genes whose expression has been associated with LINE-1 antisense promoter activity.Mobile DNA · 2023Article
- Transcription profiling of feline mammary carcinomas and derived cell lines reveals biomarkers and drug targets associated with metabolic and cell cycle pathways.Scientific reports · 2022Article
- Knockdown GTSE1 enhances radiosensitivity in non-small-cell lung cancer through DNA damage repair pathway.Journal of cellular and molecular medicine · 2020Article
- Molecular Mechanism of Hippo-YAP1/TAZ Pathway in Heart Development, Disease, and Regeneration.Frontiers in physiology · 2020Review
- GTSE1 is involved in breast cancer progression in p53 mutation-dependent manner.Journal of experimental & clinical cancer research : CR · 2019Article
- Clinical and Expression Significance of AKT1 by Co-expression Network Analysis in Endometrial Cancer.Frontiers in oncology · 2019Article
- Overexpression of TEAD4 correlates with poor prognosis of glioma and promotes cell invasion.International journal of clinical and experimental pathology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GTSE1 over-expression has been reported as a potential marker for metastasis in various types of malignancies, including breast cancer. Despite this, the transcriptional regulation of this protein and the causes of its misregulation in tumors remain largely unknown. The aims of this work were to elucidate how GTSE1 is regulated at the transcriptional level and to clarify the mechanism underlying GTSE1-dependent cell functions in triple-negative breast cancer (TNBC). Here, we identified GTSE1 as a novel target gene of the TEAD4 transcription factor, highlighting a role for the YAP and TAZ coactivators in the transcriptional regulation of GTSE1. Moreover, we found that TEAD4 controls the formation of cell protrusions required for cell migration through GTSE1, unveiling a relevant effector role for this protein in the TEAD-dependent cellular functions and confirming TEAD4 role in promoting invasion and metastasis in breast cancer. Finally, we highlighted a role for the pRb-E2F1 pathway in the control of GTSE1 transcription and observed that treatment with drugs targeting the pRb-E2F1 or YAP/TAZ-TEAD pathways dramatically downregulated the expression levels of GTSE1 and of other genes involved in the formation of metastasis, suggesting their potential use in the treatment of TNBC.
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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.