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Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance

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Veröffentlicht in: Scientific reports 7(2017) Artikel-Nummer 41138, 16 Seiten
Personen und Körperschaften: Panic, Andrej (VerfasserIn), Herskind, Carsten (VerfasserIn), Maier, Patrick (VerfasserIn)
Titel: Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance/ Andrej Panic, Julia Ketteler, Henning Reis, Ali Sak, Carsten Herskind, Patrick Maier, Herbert Rübben, Verena Jendrossek, Diana Klein
Format: E-Book-Kapitel
Sprache: Englisch
veröffentlicht:
23 January 2017
Gesamtaufnahme: : Scientific reports, 7(2017) Artikel-Nummer 41138, 16 Seiten
, volume:7
Quelle: Verbunddaten SWB
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contents Despite good treatment results in localized prostate tumors, advanced disease stages usually have a pronounced resistance to chemotherapy and radiotherapy. The membrane protein caveolin-1 (Cav1) functions here as an important oncogene. Therefore we examined the impact of stromal Cav1 expression for tumor growth and sensitivity to ionizing radiation (IR). Silencing of Cav1 expression in PC3 cells resulted in increased tumor growth and a reduced growth delay after IR when compared to tumors generated by Cav1-expressing PC3 cells. The increased radiation resistance was associated with increasing amounts of reactive tumor stroma and a Cav1 re-expression in the malignant epithelial cells. Mimicking the human situation these results were confirmed using co-implantation of Cav1-silenced PC3 cells with Cav1-silenced or Cav1-expressing fibroblasts. Immunohistochemically analysis of irradiated tumors as well as human prostate tissue specimen confirmed that alterations in stromal-epithelial Cav1 expressions were accompanied by a more reactive Cav1-reduced tumor stroma after radiation and within advanced prostate cancer tissues which potentially mediates the resistance to radiation treatment. Conclusively, the radiation response of human prostate tumors is critically regulated by Cav1 expression in stromal fibroblasts. Loss of stromal Cav1 expression in advanced tumor stages may thus contribute to resistance of these tumors to radiotherapy.
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spelling Panic, Andrej 1980- VerfasserIn (DE-588)1042166048 (DE-627)768249902 (DE-576)393724352 aut, Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance Andrej Panic, Julia Ketteler, Henning Reis, Ali Sak, Carsten Herskind, Patrick Maier, Herbert Rübben, Verena Jendrossek, Diana Klein, 23 January 2017, 16, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Gesehen am 06.06.2018, Despite good treatment results in localized prostate tumors, advanced disease stages usually have a pronounced resistance to chemotherapy and radiotherapy. The membrane protein caveolin-1 (Cav1) functions here as an important oncogene. Therefore we examined the impact of stromal Cav1 expression for tumor growth and sensitivity to ionizing radiation (IR). Silencing of Cav1 expression in PC3 cells resulted in increased tumor growth and a reduced growth delay after IR when compared to tumors generated by Cav1-expressing PC3 cells. The increased radiation resistance was associated with increasing amounts of reactive tumor stroma and a Cav1 re-expression in the malignant epithelial cells. Mimicking the human situation these results were confirmed using co-implantation of Cav1-silenced PC3 cells with Cav1-silenced or Cav1-expressing fibroblasts. Immunohistochemically analysis of irradiated tumors as well as human prostate tissue specimen confirmed that alterations in stromal-epithelial Cav1 expressions were accompanied by a more reactive Cav1-reduced tumor stroma after radiation and within advanced prostate cancer tissues which potentially mediates the resistance to radiation treatment. Conclusively, the radiation response of human prostate tumors is critically regulated by Cav1 expression in stromal fibroblasts. Loss of stromal Cav1 expression in advanced tumor stages may thus contribute to resistance of these tumors to radiotherapy., Herskind, Carsten 1952- VerfasserIn (DE-588)1028380488 (DE-627)730637409 (DE-576)375919325 aut, Maier, Patrick 1969- VerfasserIn (DE-588)1022131273 (DE-627)71692613X (DE-576)360534732 aut, Enthalten in Scientific reports [London] : Macmillan Publishers Limited, part of Springer Nature, 2011 7(2017) Artikel-Nummer 41138, 16 Seiten Online-Ressource (DE-627)663366712 (DE-600)2615211-3 (DE-576)346641179 2045-2322 nnns, volume:7 year:2017 extent:16, http://dx.doi.org/10.1038/srep41138 Verlag Resolving-System kostenfrei Volltext, https://www.nature.com/articles/srep41138 Verlag kostenfrei Volltext, http://dx.doi.org/10.1038/srep41138 LFER, LFER 2018-07-10T00:00:00Z
spellingShingle Panic, Andrej, Herskind, Carsten, Maier, Patrick, Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance, Despite good treatment results in localized prostate tumors, advanced disease stages usually have a pronounced resistance to chemotherapy and radiotherapy. The membrane protein caveolin-1 (Cav1) functions here as an important oncogene. Therefore we examined the impact of stromal Cav1 expression for tumor growth and sensitivity to ionizing radiation (IR). Silencing of Cav1 expression in PC3 cells resulted in increased tumor growth and a reduced growth delay after IR when compared to tumors generated by Cav1-expressing PC3 cells. The increased radiation resistance was associated with increasing amounts of reactive tumor stroma and a Cav1 re-expression in the malignant epithelial cells. Mimicking the human situation these results were confirmed using co-implantation of Cav1-silenced PC3 cells with Cav1-silenced or Cav1-expressing fibroblasts. Immunohistochemically analysis of irradiated tumors as well as human prostate tissue specimen confirmed that alterations in stromal-epithelial Cav1 expressions were accompanied by a more reactive Cav1-reduced tumor stroma after radiation and within advanced prostate cancer tissues which potentially mediates the resistance to radiation treatment. Conclusively, the radiation response of human prostate tumors is critically regulated by Cav1 expression in stromal fibroblasts. Loss of stromal Cav1 expression in advanced tumor stages may thus contribute to resistance of these tumors to radiotherapy.
swb_id_str 506106381
title Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance
title_auth Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance
title_full Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance Andrej Panic, Julia Ketteler, Henning Reis, Ali Sak, Carsten Herskind, Patrick Maier, Herbert Rübben, Verena Jendrossek, Diana Klein
title_fullStr Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance Andrej Panic, Julia Ketteler, Henning Reis, Ali Sak, Carsten Herskind, Patrick Maier, Herbert Rübben, Verena Jendrossek, Diana Klein
title_full_unstemmed Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance Andrej Panic, Julia Ketteler, Henning Reis, Ali Sak, Carsten Herskind, Patrick Maier, Herbert Rübben, Verena Jendrossek, Diana Klein
title_in_hierarchy Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance / Andrej Panic, Julia Ketteler, Henning Reis, Ali Sak, Carsten Herskind, Patrick Maier, Herbert Rübben, Verena Jendrossek, Diana Klein,
title_short Progression-related loss of stromal Caveolin 1 levels fosters the growth of human PC3 xenografts and mediates radiation resistance
title_sort progression related loss of stromal caveolin 1 levels fosters the growth of human pc3 xenografts and mediates radiation resistance
url http://dx.doi.org/10.1038/srep41138, https://www.nature.com/articles/srep41138