ArticleSignal transduction and targeted therapy
The β-catenin/YAP signaling axis is a key regulator of melanoma-associated fibroblasts.
Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- Endothelial PARP1 orchestrates endothelial-to-mesenchymal transition via the PARylation of FHL2 in ischaemic heart failure.Acta pharmacologica Sinica · 2026Article
- LGR5-positive fibroblasts orchestrate skin mechanoadaptation through JAK1 modulation.Nature communications · 2026Article
- YAP/TAZ inhibition refines TGF-β signaling to prevent laryngeal fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Plasticity, signaling, and metabolic rewiring in melanoma persister cells.Communications biology · 2026Review
- Mitochondrial mGPDH Modulates Fibroblast Function in Diabetic Wound Healing via the SIRT1-c-Myc-TGF-β1 Axis.Diabetes · 2026Article
- TRKB-based signature identifies high-risk squamous cell carcinoma cases and TRKB blockade reprograms tumor and stromal cells toward suppressive phenotypes.Journal of biomedical science · 2026Article
- BRAF mutation and tumor immune microenvironment in new era.American journal of cancer research · 2026Review
- PDPNCell communication and signaling : CCS · 2025Article
- Unlocking the crucial role of cancer-associated fibroblasts in tumor metastasis: Mechanisms and therapeutic prospects.Journal of advanced research · 2025Review
- Hippo/YAP signaling's multifaceted crosstalk in cancer.Frontiers in cell and developmental biology · 2025Review
- Recent advances on Hippo-YAP pathway in skin diseases.Frontiers in immunology · 2025Review
- Cell signaling inFrontiers in cellular and infection microbiology · 2025Review
- The role of Hippo/YAP1 in cancer-associated fibroblasts: Literature review and future perspectives.Cancer letters · 2024Review
- Melanoma-associated fibroblasts in tumor-promotion flammation and antitumor immunity: novel mechanisms and potential immunotherapeutic strategies.Human molecular genetics · 2024Review
- Mechanical Properties of Mouse Lung Cells and Their Effects on the Atomic Force Microscope Beam Vibrations.Cell biochemistry and biophysics · 2024Article
- YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression.Oncogene · 2024Article
- Modulating tumoral exosomes and fibroblast phenotype using nanoliposomes augments cancer immunotherapy.Science advances · 2024Article
- Alternative Wnt-signaling axis leads to a break of oncogene-induced senescence.Cell death & disease · 2024Article
- Dual effect of vitamin DBMC cancer · 2024Article
- ARID1A loss induces P4HB to activate fibroblasts to support lung cancer cell growth, invasion, and chemoresistance.Cancer science · 2024Article
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
β-catenin is a multifunctional protein that plays crucial roles in embryonic development, physiological homeostasis, and a wide variety of human cancers. Previously, we showed that in vivo targeted ablation of β-catenin in melanoma-associated fibroblasts after melanoma formation significantly suppressed tumor growth. However, when the expression of β-catenin was ablated in melanoma-associated fibroblasts before tumor initiation, melanoma development was surprisingly accelerated. How stromal β-catenin deficiency leads to opposite biological effects in melanoma progression is not completely understood. Here, we report that β-catenin is indispensable for the activation of primary human stromal fibroblasts and the mediation of fibroblast-melanoma cell interactions. Using coimmunoprecipitation and proximity ligation assays, we identified Yes-associated protein (YAP) as an important β-catenin-interacting partner in stromal fibroblasts. YAP is highly expressed in the nuclei of cancer-associated fibroblasts (CAFs) in both human and murine melanomas. Mechanistic investigation revealed that YAP nuclear translocation is significantly modulated by Wnt/β-catenin activity in fibroblasts. Blocking Wnt/β-catenin signaling in stromal fibroblasts inhibited YAP nuclear translocation. In the absence of YAP, the ability of stromal fibroblasts to remodel the extracellular matrix (ECM) was inhibited, which is consistent with the phenotype observed in cells with β-catenin deficiency. Further studies showed that the expression of ECM proteins and enzymes required for remodeling the ECM was suppressed in stromal fibroblasts after YAP ablation. Collectively, our data provide a new paradigm in which the β-catenin-YAP signaling axis regulates the activation and tumor-promoting function of stromal fibroblasts.
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