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侵袭性卵巢肿瘤产生的恶性腹水的促血管生成能力。

The Proangiogenic Capabilities of Malignant Ascites Generated by Aggressive Ovarian Tumors.

机构信息

Department of Hypertensiology, Angiology and Internal Medicine, Poznań University of Medical Sciences, Długa 1/2 Str., 61-848 Poznań, Poland.

Division of Gynecological Surgery, Poznań University of Medical Sciences, Polna 33 Str., 60-535 Poznań, Poland.

出版信息

Biomed Res Int. 2017;2017:2592496. doi: 10.1155/2017/2592496. Epub 2017 Sep 20.

DOI:10.1155/2017/2592496
PMID:29085834
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5632494/
Abstract

Here we examined whether malignant ascites may determine ovarian tumor angiogenesis, and if so whether ascites generated by highly aggressive serous and undifferentiated cancers are more proangiogenic than those from less aggressive clear cell and endometrioid tumors. Angiogenesis was analyzed according to expression of CD31, CD34, and connexin 43. Proliferation and migration of endothelial cells were tested using fluorescence-based methods. The quantification of angiogenic agents and hypoxia-inducible factor 1 (HIF-1) was performed using specific immunoassays. Results showed that the expression of CD31 and CD34 in serous and undifferentiated tumors was greater, whereas endothelial expression of connexin 43 was lower than in clear cell and endometrioid lesions. Serous cancers that formed in the presence of ascites displayed increased expression of connexin 43 in vascular smooth muscles as compared with tumors developed in the fluid's absence. Endothelial cells exposed to ascites from serous and undifferentiated tumors proliferated and migrated more vigorously than cells subjected to ascites from clear cell and endometrioid cancers. They also exhibited an increased level of HIF-1 and produced increased amounts of multiple proangiogenic agents. Our results indicate that high vascularization of aggressive ovarian tumors may be associated with profound angiogenic capabilities of ascites generated by these tumors.

摘要

在这里,我们研究了恶性腹水是否会决定卵巢肿瘤的血管生成,如果是,那么高度侵袭性的浆液性和未分化癌症产生的腹水是否比低度侵袭性的透明细胞和子宫内膜样肿瘤产生的腹水更具血管生成能力。血管生成根据 CD31、CD34 和连接蛋白 43 的表达进行分析。使用荧光法测试内皮细胞的增殖和迁移。使用特定的免疫测定法对血管生成剂和缺氧诱导因子 1(HIF-1)的定量进行了检测。结果表明,浆液性和未分化肿瘤中 CD31 和 CD34 的表达更高,而内皮细胞连接蛋白 43 的表达低于透明细胞和子宫内膜样病变。在存在腹水的情况下形成的浆液性癌症与在没有腹水的情况下形成的肿瘤相比,血管平滑肌中连接蛋白 43 的表达增加。与暴露于透明细胞和子宫内膜样癌腹水的细胞相比,暴露于浆液性和未分化肿瘤腹水的内皮细胞增殖和迁移更为活跃。它们还表现出更高水平的 HIF-1,并产生更多的多种促血管生成剂。我们的结果表明,侵袭性卵巢肿瘤的高血管化可能与这些肿瘤产生的腹水具有深远的血管生成能力有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/7e2f1b5bc853/BMRI2017-2592496.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/f93c87752de2/BMRI2017-2592496.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/63b15191b505/BMRI2017-2592496.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/68aa7710ed0f/BMRI2017-2592496.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/ec309cec8d67/BMRI2017-2592496.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/7e2f1b5bc853/BMRI2017-2592496.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/f93c87752de2/BMRI2017-2592496.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/63b15191b505/BMRI2017-2592496.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/68aa7710ed0f/BMRI2017-2592496.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/ec309cec8d67/BMRI2017-2592496.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4c9/5632494/7e2f1b5bc853/BMRI2017-2592496.005.jpg

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Ovarian cancer ascites enhance the migration of patient-derived peritoneal mesothelial cells via cMet pathway through HGF-dependent and -independent mechanisms.
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Int J Mol Sci. 2021 Apr 19;22(8):4222. doi: 10.3390/ijms22084222.
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The Epithelial-Mesenchymal Transition Initiated by Malignant Ascites Underlies the Transmesothelial Invasion of Ovarian Cancer Cells.恶性腹水引发的上皮-间充质转化是卵巢癌细胞穿破间皮的基础。
Int J Mol Sci. 2019 Jan 2;20(1):137. doi: 10.3390/ijms20010137.
卵巢癌腹水通过 HGF 依赖性和非依赖性机制通过 cMet 途径增强患者来源的腹膜间皮细胞的迁移。
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