ArticleThe Journal of biological chemistry2014
The transcriptional regulators TAZ and YAP direct transforming growth factor β-induced tumorigenic phenotypes in breast cancer cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 1 of them a synthesis that pooled it.
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
146 citing papers in PubMed, 1 synthesis or guideline pooled it, 229 citations in OpenAlex.
- Prognostic and clinicopathological role of long non-coding RNA UCA1 in various carcinomas.Oncotarget · 2017Pooled it
- Review
- Targeting the neurovascular unit in retinal fibrosis: mechanisms and therapeutic perspectives.Frontiers in medicine · 2026Review
- ANTXR1 blockade enhances cardiac function in preclinical models of heart failure.Nature cardiovascular research · 2025Article
- Exploring the molecular mechanism of icariin improving spinal cord injury through network pharmacology combined with experimental verification.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- YAP acts as an independent prognostic marker and regulates growth and metastasis of gastrointestinal stromal tumors via FBXW7-YAP pathway.Journal of gastroenterology · 2025Article
- Investigating combined hypoxia and stemness indices for prognostic transcripts in gastric cancer: Machine learning and network analysis approaches.Biochemistry and biophysics reports · 2025Article
- Decoding gene expression profiles of Hippo signaling pathway components in breast cancer.Molecular biology reports · 2025Article
- Transcription coactivator YAP1 promotes CCND1/CDK6 expression, stimulating cell proliferation in cloned cattle placentas.Zoological research · 2025Article
- MAFF inhibits angiogenesis in non-small cell lung cancer by suppressing YAP1 nuclear translocation.PeerJ · 2025Article
- Hippo/YAP signaling's multifaceted crosstalk in cancer.Frontiers in cell and developmental biology · 2025Review
- The role of YAP/TAZ mechanosignaling in trabecular meshwork and Schlemm's canal cell dysfunction.Vision research · 2024Review
- Lung injury-induced activated endothelial cell states persist in aging-associated progressive fibrosis.Nature communications · 2024Article
- Article
- YAP promotes the early development of temporomandibular joint bony ankylosis by regulating mesenchymal stem cell function.Scientific reports · 2024Article
- Generation of human alveolar epithelial type I cells from pluripotent stem cells.Cell stem cell · 2024Article
- The Role of Urothelial Cancer-Associated 1 in Gynecological Cancers.Current issues in molecular biology · 2024Review
- Article
- Targeting SMAD-Dependent Signaling: Considerations in Epithelial and Mesenchymal Solid Tumors.Pharmaceuticals (Basel, Switzerland) · 2024Review
- TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma.Frontiers in immunology · 2024Review
86 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Uncontrolled transforming growth factor-β (TGFβ) signaling promotes aggressive metastatic properties in late-stage breast cancers. However, how TGFβ-mediated cues are directed to induce tumorigenic events is poorly understood, particularly given that TGFβ has clear tumor suppressing activity in other contexts. Here, we demonstrate that the transcriptional regulators TAZ and YAP (TAZ/YAP), key effectors of the Hippo pathway, are necessary to promote and maintain TGFβ-induced tumorigenic phenotypes in breast cancer cells. Interactions between TAZ/YAP, TGFβ-activated SMAD2/3, and TEAD transcription factors reveal convergent roles for these factors in the nucleus. Genome-wide expression analyses indicate that TAZ/YAP, TEADs, and TGFβ-induced signals coordinate a specific pro-tumorigenic transcriptional program. Importantly, genes cooperatively regulated by TAZ/YAP, TEAD, and TGFβ, such as the novel targets NEGR1 and UCA1, are necessary for maintaining tumorigenic activity in metastatic breast cancer cells. Nuclear TAZ/YAP also cooperate with TGFβ signaling to promote phenotypic and transcriptional changes in nontumorigenic cells to overcome TGFβ-repressive effects. Our work thus identifies cross-talk between nuclear TAZ/YAP and TGFβ signaling in breast cancer cells, revealing novel insight into late-stage disease-driving mechanisms.
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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.