ArticleOncogene2017
RAC-LATS1/2 signaling regulates YAP activity by switching between the YAP-binding partners TEAD4 and RUNX3.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 65 citations in OpenAlex.
- Actin Branching Regulates Cell Spreading and Force on Talin, but not Activation of YAP.Cellular and molecular bioengineering · 2025Article
- Natural compound PEITC inhibits gain of function of p53 mutants in cancer cells by switching YAP-binding partners between p53 and p73.Acta pharmacologica Sinica · 2025Article
- YAP controls cell migration and invasion through a Rho GTPase switch.Science signaling · 2025Article
- Expression of Yes-associated protein in endothelial cells of human corneas before and after storage in organ culture.Scientific reports · 2024Article
- CRKL Enhances YAP Signaling through Binding and JNK/JUN Pathway Activation in Liver Cancer.International journal of molecular sciences · 2024Article
- Investigation of YAP-1, OTX-2, and nestin protein expressions in neuroblastoma: a preliminary study.Annals of clinical and translational neurology · 2024Article
- The Wnt-dependent and Wnt-independent functions of BCL9 in development, tumorigenesis, and immunity: Implications in therapeutic opportunities.Genes & diseases · 2024Review
- Thrombospondin 1 and Reelin act through Vldlr to regulate cardiac growth and repair.Basic research in cardiology · 2024Article
- The TGFβ→TAK1→LATS→YAP1 Pathway Regulates the Spatiotemporal Dynamics of YAP1.Molecules and cells · 2023Article
- Aberrant MET activation impairs perinuclear actin cap organization with YAP1 cytosolic relocation.Communications biology · 2023Article
- Key role for Rac in the early transcriptional response to extracellular matrix stiffness and stiffness-dependent repression of ATF3.Journal of cell science · 2023Article
- Transcriptomic Context ofBiomedicines · 2023Article
- The Hippo signaling pathway in gastric cancer.Acta biochimica et biophysica Sinica · 2023Review
- YAP 5-methylcytosine modification increases its mRNA stability and promotes the transcription of exosome secretion-related genes in lung adenocarcinoma.Cancer gene therapy · 2023Article
- Review
- Targeting the Hippo/YAP/TAZ signalling pathway: Novel opportunities for therapeutic interventions into skin cancers.Experimental dermatology · 2022Review
- The clinicopathological and prognostic significances of LATS1 expression in breast cancer.Histology and histopathology · 2022Article
- Molecular regulation of trophoblast stem cell self-renewal and giant cell differentiation by the Hippo components YAP and LATS1.Stem cell research & therapy · 2022Article
- Hippo in Gastric Cancer: From Signalling to Therapy.Cancers · 2022Review
- TEAD4 as an Oncogene and a Mitochondrial Modulator.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor-suppressor RUNX3 has a critical role in a lineage determination, cell cycle arrest and apoptosis. Lozenge (Lz), a Drosophila homolog of mammalian RUNX family members, has integral roles in these processes and specifically in eye cell fate determination. To elucidate the genetic modifiers of Lz/RUNX3, we performed a large-scale functional screen in a fly mutant library. The screen revealed genetic interactions between the Lz, Rac and Hippo pathways. Analysis of interactions among these genes revealed that the defective phenotype resulting from activation of Yki, an end point effector of the Hippo pathway, was suppressed by Lz and enhanced by Rac-Trio. Molecular biological analysis using mammalian homologs reveled that LATS1/2-mediated YAP phosphorylation-facilitated dissociation of the YAP-TEAD4 complex and association of the YAP-RUNX3 complex. When cells were stimulated to proliferate, activated RAC-TRIO signaling inhibited LATS1/2-mediated YAP phosphorylation; consequently, YAP dissociated from RUNX3 and associated with TEAD, thereby replacing the YAP-RUNX3 complex with YAP-TEAD. RUNX3 contributed to both association and dissociation of YAP-TEAD complex, most likely through the formation of the YAP-TEAD-RUNX3 ternary complex. Ectopic expression of RUNX3 in MKN28 gastric cancer cells reduced tumorigenicity, and the tumor-suppressive activity of RUNX3 was associated with its ability to interact with YAP. These results identify a novel regulatory mechanism, mediated by the Hippo and RAC-TRIO pathways, that changes the binding partner of YAP.
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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.