ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Targeted deactivation of cancer-associated fibroblasts by β-catenin ablation suppresses melanoma growth.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Uncovering the Intricate and Heterogeneous Cellular Microenvironment of Cutaneous Melanoma.Medicina (Kaunas, Lithuania) · 2026Review
- A Fucose-Containing Sulfated Polysaccharide from Spatoglossum schröederi Potentially Targets Tumor Growth Rather Than Cytotoxicity: Distinguishing Action on Human Melanoma Cell Lines.Marine biotechnology (New York, N.Y.) · 2024Article
- Review
- CAFs targeted ultrasound-responsive nanodroplets loaded V9302 and GLULsiRNA to inhibit melanoma growth via glutamine metabolic reprogramming and tumor microenvironment remodeling.Journal of nanobiotechnology · 2023Article
- Fibroblasts as Turned Agents in Cancer Progression.Cancers · 2023Review
- Thyroid Cancer and Fibroblasts.Cancers · 2022Review
- Induction of Pro-Fibrotic CLIC4 in Dermal Fibroblasts by TGF-β/Wnt3a Is Mediated by GLI2 Upregulation.Cells · 2022Article
- Acidic and Hypoxic Microenvironment in Melanoma: Impact of Tumour Exosomes on Disease Progression.Cells · 2021Review
- Fundamental and Clinical Applications of Materials Based on Cancer-Associated Fibroblasts in Cancers.International journal of molecular sciences · 2021Review
- Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer.Signal transduction and targeted therapy · 2021Review
- Article
- Stromal Cells Present in the Melanoma Niche Affect Tumor Invasiveness and Its Resistance to Therapy.International journal of molecular sciences · 2021Review
- A Framework of Major Tumor-Promoting Signal Transduction Pathways Implicated in Melanoma-Fibroblast Dialogue.Cancers · 2020Review
- Tumor Microenvironment: Implications in Melanoma Resistance to Targeted Therapy and Immunotherapy.Cancers · 2020Review
- The Role of Dermal Fibroblasts in Nevoid Basal Cell Carcinoma Syndrome Patients: An Overview.International journal of molecular sciences · 2020Review
- Preclinical investigation of ovatodiolide as a potential inhibitor of colon cancer stem cells via downregulating sphere-derived exosomal β-catenin/STAT3/miR-1246 cargoes.American journal of cancer research · 2020Article
- Article
- The Role of Tumor Microenvironment in Chemoresistance: 3D Extracellular Matrices as Accomplices.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblasts (CAFs) are the crucial components of the dynamic tumor microenvironment, which not only supports the growth and metastasis of melanoma but also contributes to drug resistance in melanoma treatment. We recently discovered that loss of β-catenin signaling deactivated stromal fibroblasts and reduced the production of paracrine factors and extracellular matrix proteins. Based on this finding, we aimed to determine whether melanoma growth could be suppressed by targeted deactivation of CAFs via β-catenin ablation using a combination of in vitro and in vivo approaches. Using an in vitro three-dimensional (3D) tumor co-culture model, we showed that β-catenin-deficient fibroblasts lost the ability to respond to melanoma cell stimulation and to support the growth of B16F10 melanoma cells. To determine the in vivo effects of CAF deactivation on melanoma growth, we designed a novel genetic approach to ablate β-catenin expression in melanoma-associated fibroblasts only after melanoma tumor was formed. As expected, our observation showed that development of B16F10 melanoma was significantly delayed when β-catenin expression was ablated in CAFs. We determined that inhibition of tumor growth was due to decreased melanoma cell proliferation and increased cell death. Further analysis revealed that CAF deactivation caused the downregulation of the MAPK/ERK signaling cascade and S and G2/M phase cell cycle arrest in B16F10 melanoma cells. Overall, our data emphasize the significance of targeting CAFs as a potential novel therapeutic approach to improve melanoma treatment by creating a tumor-suppressive microenvironment through tumor-stroma interactions.
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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.