ArticleOncogenesis2015
Endothelial Caveolin-1 regulates the radiation response of epithelial prostate tumors.
Article in Oncogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Senescent fibroblasts modulate the radiation response of neighboring epithelial cells.Cell death discovery · 2025Article
- Prostate cancer microenvironment: multidimensional regulation of immune cells, vascular system, stromal cells, and microbiota.Molecular cancer · 2024Review
- Endothelial Cell Response to Combined Photon or Proton Irradiation with Doxorubicin.International journal of molecular sciences · 2023Article
- "Stromal cells in prostate cancer pathobiology: friends or foes?"British journal of cancer · 2023Review
- Similar additive effects of doxorubicin in combination with photon or proton irradiation in soft tissue sarcoma models.Frontiers in oncology · 2023Article
- Stromal Reprogramming by FAK Inhibition Overcomes Radiation Resistance to Allow for Immune Priming and Response to Checkpoint Blockade.Cancer discovery · 2022Article
- Cancer-associated fibroblast-derived gene signatures predict radiotherapeutic survival in prostate cancer patients.Journal of translational medicine · 2022Article
- Alteration of cholesterol distribution at the plasma membrane of cancer cells: From evidence to pathophysiological implication and promising therapy strategy.Frontiers in physiology · 2022Review
- Stromal Fibroblasts Counteract the Caveolin-1-Dependent Radiation Response of LNCaP Prostate Carcinoma Cells.Frontiers in oncology · 2022Article
- Role of caveolin-1 as a biomarker for radiation resistance and tumor aggression in lung cancer.PloS one · 2021Article
- The tumor microenvironment and radiotherapy response; a central role for cancer-associated fibroblasts.Clinical and translational radiation oncology · 2020Review
- Caveolin-1 regulates the ASMase/ceramide-mediated radiation response of endothelial cells in the context of tumor-stroma interactions.Cell death & disease · 2020Article
- Host CD39 Deficiency Affects Radiation-Induced Tumor Growth Delay and Aggravates Radiation-Induced Normal Tissue Toxicity.Frontiers in oncology · 2020Article
- Progression-Related Loss of Stromal Caveolin 1 Levels Mediates Radiation Resistance in Prostate Carcinoma via the Apoptosis Inhibitor TRIAP1.Journal of clinical medicine · 2019Article
- Impact of Cancer-Associated Fibroblast on the Radiation-Response of Solid Xenograft Tumors.Frontiers in molecular biosciences · 2019Article
- Association of caveolin-1 protein expression with hepatocellular carcinoma: a meta-analysis and literature review.Cancer management and research · 2019Article
- Cellular Constituents of the Prostate Stroma: Key Contributors to Prostate Cancer Progression and Therapy Resistance.Cold Spring Harbor perspectives in medicine · 2018Review
- The Tumor Vascular Endothelium as Decision Maker in Cancer Therapy.Frontiers in oncology · 2018Review
- Mesenchymal Stem Cell Therapy Protects Lungs from Radiation-Induced Endothelial Cell Loss by Restoring Superoxide Dismutase 1 Expression.Antioxidants & redox signaling · 2017Article
- Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The membrane protein caveolin-1 (Cav1) recently emerged as a novel oncogene involved in prostate cancer progression with opposed regulation in epithelial tumor cells and the tumor stroma. Here we examined the role of stromal Cav1 for growth and radiation response of MPR31-4 prostate cancer xenograft tumors using Cav1-deficient C57Bl/6 mice. Syngeneic MPR31-4 tumors grew faster when implanted into Cav1-deficient mice. Increased tumor growth on Cav1-deficient mice was linked to decreased integration of smooth muscle cells into the wall of newly formed blood vessels and thus with a less stabilized vessel phenotype compared with tumors from Cav1 wild-type animals. However, tumor growth delay of MPR31-4 tumors grown on Cav1 knockout mice to a single high-dose irradiation with 20 Gray was more pronounced compared with tumors grown on wild-type mice. Increased radiation-induced tumor growth delay in Cav1-deficient mice was associated with an increased endothelial cell apoptosis. In vitro studies using cultured endothelial cells (ECs) confirmed that the loss of Cav1 expression increases sensitivity of ECs to radiation-induced apoptosis and reduces their clonogenic survival after irradiation. Immunohistochemical analysis of human tissue specimen further revealed that although Cav1 expression is mostly reduced in the tumor stroma of advanced and metastatic prostate cancer, the vascular compartment still expresses high levels of Cav1. In conclusion, the radiation response of MPR31-4 prostate tumors is critically regulated by Cav1 expression in the tumor vasculature. Thus, Cav1 might be a promising therapeutic target for combinatorial therapies to counteract radiation resistance of prostate cancer at the level of the tumor vasculature.
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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.