ArticleScientific reports2017
VGLL4 Selectively Represses YAP-Dependent Gene Induction and Tumorigenic Phenotypes in Breast Cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- Coupling Vgll4b/Yap-regulated posterior cell addition with anterior vacuolation enables robust notochord elongation.Development (Cambridge, England) · 2026Article
- Systematic analysis of hippo pathway signaling identifies TEAD1 as a transcriptional regulator of neuroendocrine prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- Two distinct modes of Vgll4-mediated Tead regulation control organ size in zebrafish.Communications biology · 2026Article
- FOS gene fusions in osteosarcoma raise the hypothesis of malignant transformation of osteoblastoma.Virchows Archiv : an international journal of pathology · 2026Article
- Vestigial-like 4 Regulates Neurogenesis and Neural Crest Formation DuringJournal of developmental biology · 2026Article
- NCAPH-YAP1 interaction promotes breast cancer stemness and tumor progression.Stem cell research & therapy · 2025Article
- TEAD-targeting small molecules induce a cofactor switch to regulate the Hippo pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Emerging mechanomedicines informed by mechanotransduction along the integrin-cytoskeleton-nucleus axis.APL bioengineering · 2025Review
- YAP/TAZ as mechanobiological signaling pathway in cardiovascular physiological regulation and pathogenesis.Mechanobiology in medicine · 2024Article
- YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024Review
- Clinical Significance and Expression Pattern of RIP5 and VGLL4 in Clear Cell Renal Cell Carcinoma Patients Treated with Sunitinib.Biomedicines · 2024Article
- VGLL4 promotes vascular endothelium specification via TEAD1 in the vascular organoids and human pluripotent stem cells-derived endothelium model.Cellular and molecular life sciences : CMLS · 2023Article
- New insights into the ambivalent role of YAP/TAZ in human cancers.Journal of experimental & clinical cancer research : CR · 2023Review
- The oncogenic roles and clinical implications of YAP/TAZ in breast cancer.British journal of cancer · 2023Review
- Leveraging Hot Spots of TEAD-Coregulator Interactions in the Design of Direct Small Molecule Protein-Protein Interaction Disruptors Targeting Hippo Pathway Signaling.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Lycorine weakens tamoxifen resistance of breast cancer via abrogating HAGLR-mediated epigenetic suppression on VGLL4 by DNMT1.The Kaohsiung journal of medical sciences · 2023Article
- Collagen VI expression is negatively mechanosensitive in pancreatic cancer cells and supports the metastatic niche.Journal of cell science · 2022Article
- Recurrent VGLL3 fusions define a distinctive subset of spindle cell rhabdomyosarcoma with an indolent clinical course and striking predilection for the head and neck.Genes, chromosomes & cancer · 2022Article
- Integrating Genetic Alterations and the Hippo Pathway in Head and Neck Squamous Cell Carcinoma for Future Precision Medicine.Journal of personalized medicine · 2022Review
- HOXB13 suppresses proliferation, migration and invasion, and promotes apoptosis of gastric cancer cells through transcriptional activation of VGLL4 to inhibit the involvement of TEAD4 in the Hippo signaling pathway.Molecular medicine reports · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Members of the mammalian Vestigial-like (VGLL) family of transcriptional cofactors activate genes in response to a wide variety of environmental cues. Recently, VGLL proteins have been proposed to regulate key signaling networks involved in cancer development and progression. However, the biological and clinical significance of VGLL dysregulation in human breast cancer pathogenesis remains unknown. Here, we report that diminished VGLL4 expression, but not VGLL1-3, correlated with both shorter relapse-free survival and shorter disease-specific survival of cancer patients with different molecular subtypes of breast cancer. Additionally, we further demonstrate that overexpression of VGLL4 reduces breast cancer cell proliferation, migration, intravasation/extravasation potential, favors cell death, and suppresses tumor growth in vivo. Mechanistically, VGLL4 negatively regulates the TEAD1-YAP1 transcriptional complex and exerts its growth inhibitory control through its evolutionary conserved TDU2 domain at its C-terminus. The results suggest that VGLL4 is a candidate tumor suppressor gene which acts by selectively antagonizing YAP-dependent tumor growth. VGLL4 may be a promising therapeutic target in breast cancer.
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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.