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与进展相关的基质 Cav-1 水平丧失促进了人 PC3 异种移植物的生长，并介导了辐射抗性。

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

机构信息

Institute of Cell Biology (Cancer Research), University of Duisburg-Essen, University Hospital, Virchowstrasse 173, 45122 Essen, Germany.

Department of Urology and Urooncology, University of Duisburg-Essen, University Hospital, Essen, Hufelandstr. 55, 45122 Essen, Germany.

出版信息

Sci Rep. 2017 Jan 23;7:41138. doi: 10.1038/srep41138.

DOI:10.1038/srep41138
PMID:28112237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5255553/
Abstract

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.

摘要

尽管局部前列腺肿瘤的治疗效果良好，但晚期疾病通常对化疗和放疗有明显的耐药性。膜蛋白窖蛋白-1（Cav1）在此作为重要的癌基因发挥作用。因此，我们研究了基质 Cav1 表达对肿瘤生长和对电离辐射（IR）敏感性的影响。与 Cav1 表达的 PC3 细胞生成的肿瘤相比，沉默 PC3 细胞中的 Cav1 表达导致肿瘤生长增加和 IR 后生长延迟减少。增加的辐射抗性与反应性肿瘤基质的增加以及恶性上皮细胞中 Cav1 的重新表达有关。通过将 Cav1 沉默的 PC3 细胞与 Cav1 沉默或 Cav1 表达的成纤维细胞共植入来模拟人类情况，证实了这些结果。对辐照肿瘤以及人前列腺组织标本的免疫组织化学分析证实，基质-上皮 Cav1 表达的改变伴随着辐射后更具反应性的 Cav1 减少的肿瘤基质，并且在晚期前列腺癌组织内，这可能介导对放射治疗的抵抗。总之，人前列腺肿瘤的放射反应受到基质成纤维细胞中 Cav1 表达的严格调节。因此，晚期肿瘤中基质 Cav1 表达的丧失可能导致这些肿瘤对放疗的抵抗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/e3991084e678/srep41138-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/455ded73a9e2/srep41138-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/ec56610c6dca/srep41138-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/71b18a761a83/srep41138-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/cd0525017c06/srep41138-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/5bdaa9d08b2f/srep41138-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/ca572b808c12/srep41138-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/27b5cd00fd69/srep41138-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/e3991084e678/srep41138-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/455ded73a9e2/srep41138-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/ec56610c6dca/srep41138-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/71b18a761a83/srep41138-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/cd0525017c06/srep41138-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/5bdaa9d08b2f/srep41138-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/ca572b808c12/srep41138-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/27b5cd00fd69/srep41138-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1833/5255553/e3991084e678/srep41138-f8.jpg

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