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The clinical relevance of the tumor microenvironment in modulating the response of solid tumors to chemotherapy and radiotherapy has been documented. Herein, the membrane protein caveolin-1 (Cav1) came into focus as it is overexpressed or mutated in solid human tumors, e.g. prostate or breast cancer, and regulates several signaling processes and cellular functions with significance for the survival of cancer cells including resistance-promoting interactions with extracellular matrix proteins, tumor angiogenesis and metastasis at advanced tumor stages. However the role of Cav1 for the outcome of radiotherapy is still largely unknown, particularly in the context of tumor stroma interactions. In the proposed project we will explore the role played by Cav1 in the regulation of DNA-damage induction, DNA repair, and cell fate in response to ionizing radiation (IR) in vitro by using genetically modified syngeneic pairs of cancer cells, endothelial cells or fibroblasts with altered Cav1 expression. We will also use genetic approaches to address the role of Cav1 posttranslational modifications and of cancer-associated mutations for the cellular response to ionizing radiation. Moreover we will define signaling pathways that integrate Cav1 into the DNA damage response and cell-fate decisions upon IR. Finally, we will dissect Cav1-driven resistance-promoting tumor stroma interactions in vitro and in vivo in murine models. Our investigations shall foster the development of new therapeutic strategies to target stroma-mediated radiation resistance.
The clinical relevance of the tumor microenvironment in modulating the response of solid tumors to chemotherapy and radiotherapy has been documented. Herein, the membrane protein caveolin-1 (Cav1) came into focus as it is overexpressed or mutated in solid human tumors, e.g. prostate or breast cancer, and regulates several signaling processes and cellular functions with significance for the survival of cancer cells including resistance-promoting interactions with extracellular matrix proteins, tumor angiogenesis and metastasis at advanced tumor stages. However the role of Cav1 for the outcome of radiotherapy is still largely unknown, particularly in the context of tumor stroma interactions. In the proposed project we will explore the role played by Cav1 in the regulation of DNA-damage induction, DNA repair, and cell fate in response to ionizing radiation (IR) in vitro by using genetically modified syngeneic pairs of cancer cells, endothelial cells or fibroblasts with altered Cav1 expression. We will also use genetic approaches to address the role of Cav1 posttranslational modifications and of cancer-associated mutations for the cellular response to ionizing radiation. Moreover we will define signaling pathways that integrate Cav1 into the DNA damage response and cell-fate decisions upon IR. Finally, we will dissect Cav1-driven resistance-promoting tumor stroma interactions in vitro and in vivo in murine models. Our investigations shall foster the development of new therapeutic strategies to target stroma-mediated radiation resistance.
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Frontiers in Oncology (2024)
Frontiers in Immunology (2023)
crossref(2023)
crossref(2023)
Frontiers in immunology (2023): 1227191
STRAHLENTHERAPIE UND ONKOLOGIE (2023): S173-S173
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Sophia A Hogh-Binder,Diana Klein, Frederik Wolfsperger,Stephan M Huber,Jörg Hennenlotter,Arnulf Stenzl,Justine Rudner
Cancersno. 9 (2023): 2496
Frontiers in Oncology (2023): 1211984-1211984
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