ArticleMolecular and cellular biology2016
Fibroblast Growth Factor Receptor-Dependent and -Independent Paracrine Signaling by Sunitinib-Resistant Renal Cell Carcinoma.
Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Establishment of patient-derived xenografts for neuroendocrine tumors in the avian embryo model.Endocrine-related cancer · 2026Article
- Lipid-Based Nanoparticles in Cancer Therapy: Advances in Targeted Drug Delivery and Therapeutic Potential for Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Hsa_circ_0072732 enhances sunitinib resistance of renal cell carcinoma by inhibiting ferroptosis.Discover oncology · 2024Article
- Curcumin Inhibits Proliferation of Renal Cell Carcinoma in vitro and in vivo by Regulating miR-148/ADAMTS18 through Suppressing Autophagy.Chinese journal of integrative medicine · 2023Article
- Microphysiological model of renal cell carcinoma to inform anti-angiogenic therapy.Biomaterials · 2022Article
- Advances in Renal Cell Carcinoma Drug Resistance Models.Frontiers in oncology · 2022Review
- Multi-Omics Investigations Revealed Underlying Molecular Mechanisms Associated With Tumor Stiffness and Identified Sunitinib as a Potential Therapy for Reducing Stiffness in Pituitary Adenomas.Frontiers in cell and developmental biology · 2022Article
- Curcumin reverses the sunitinib resistance in clear cell renal cell carcinoma (ccRCC) through the induction of ferroptosis via theTranslational cancer research · 2021Article
- Determinants of resistance to VEGF-TKI and immune checkpoint inhibitors in metastatic renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2021Review
- A New Antitumor Direction: Tumor-Specific Endothelial Cells.Frontiers in oncology · 2021Review
- Update on Circulating Tumor Cells in Genitourinary Tumors with Focus on Prostate Cancer.Cells · 2020Review
- Drug resistance in papillary RCC: from putative mechanisms to clinical practicalities.Nature reviews. Urology · 2019Review
- Resistance to Systemic Agents in Renal Cell Carcinoma Predict and Overcome Genomic Strategies Adopted by Tumor.Cancers · 2019Review
- A 3D Human Renal Cell Carcinoma-on-a-Chip for the Study of Tumor Angiogenesis.Neoplasia (New York, N.Y.) · 2018Article
- Modeling Renal Cell Carcinoma in Mice:Cancer discovery · 2017Article
- Less is more: low expression of MT1-MMP is optimal to promote migration and tumourigenesis of breast cancer cells.Molecular cancer · 2016Article
- FGFs: crucial factors that regulate tumour initiation and progression.Cell proliferation · 2016Review
- The current role of cytoreductive nephrectomy for metastatic renal cell carcinoma.Indian journal of urology : IJU : journal of the Urological Society of IndiaReview
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Antiangiogenic therapies, such as sunitinib, have revolutionized renal cell carcinoma (RCC) treatment. However, a precarious understanding of how resistance emerges and a lack of tractable experimental systems hinder progress. We evaluated the potential of primary RCC cultures (derived from tumors and tumor grafts) to signal to endothelial cells (EC) and fibroblasts in vitro and to stimulate angiogenesis ex vivo in chorioallantoic membrane (CAM) assays. From 65 patients, 27 primary cultures, including several from patients with sunitinib-resistant RCC, were established. RCC cells supported EC survival in coculture assays and induced angiogenesis in CAM assays. RCC-induced EC survival was sensitive to sunitinib in half of the tumors and was refractory in tumors from resistant patients. Sunitinib sensitivity correlated with vascular endothelial growth factor (VEGF) production. RCC induced paracrine extracellular signal-regulated kinase (ERK) activation in EC which was inhibited by sunitinib in sensitive but not in resistant tumors. As determined by fibroblast growth factor receptor substrate 2 (FRS2) phosphorylation in fibroblasts, RCC broadly induced low-level fibroblast growth factor receptor (FGFR) signaling. Whereas ERK activation in EC was uniformly inhibited by combined VEGF/platelet-derived growth factor (PDGF)/FGF receptor inhibitors, paracrine ERK activation in fibroblasts was blocked in only a fraction of tumors. Our data show that RCC activates EC through VEGF-dependent and -independent pathways, that sunitinib sensitivity correlates with VEGF-mediated ERK activation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signaling in EC but not in fibroblasts.
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