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10.18632/oncotarget.24626 http://scihub22266oqcxt.onion/10.18632/oncotarget.24626 C5929404!5929404 !29731961     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29731961 &cmd=llinks): Failed to open stream: HTTP request failed! 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Macrophages induce "budding" in aggressive human colon cancer subtypes by protease-mediated disruption of tight junctions |pdf=|usr=}}{{29731961 }} gab.com Text Macrophages induce "budding" in aggressive human colon cancer subtypes by protease-mediated disruption of tight junctions JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29731961 #FOAvip Primary human colorectal tumors with a high stromal content have an increased capacity to metastasize. Cancer-associated fibroblasts (CAFs) promote metastasis, but the contribution of other stromal cell types is unclear. Here we searched for additional stromal cell types that contribute to aggressive tumor cell behavior. By making use of the 'immunome compendium'-a collection of gene signatures reflecting the presence of specific immune cell-types-we show that macrophage signatures are most strongly associated with a high CAF content and with poor prognosis in multiple large cohorts of primary tumors and liver metastases. Co-culturing macrophages with patient-derived colonospheres promoted 'budding' of small clusters of tumor cells from the bulk. Immunohistochemistry showed that budding tumor clusters in stroma-rich areas of T1 colorectal carcinomas were surrounded by macrophages. In vitro budding was accompanied by reduced levels of the tight junction protein occludin, but OCLN mRNA levels did not change, nor did markers of epithelial mesenchymal transition. Budding was accompanied by nuclear accumulation of ?-catenin, which was also observed in budding tumor cell clusters in situ. The NF?B inhibitor Sanguinarine resulted in a decrease in MMP7 protein expression and both NF?B inhibitor Sanguinarine and MMP inhibitor Batimastat prevented occludin degradation and budding. We conclude that macrophages contribute to the aggressive nature of stroma-rich colon tumors by promoting an MMP-dependent pathway that operates in parallel to classical EMT and leads to tight junction disruption. Twit Text FOAVip Macrophages induce "budding" in aggressive human colon cancer subtypes by protease-mediated disruption of tight junctions ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29731961 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29731961 #FOAvip English Wikipedia <ref>{{Cite pmid|29731961 }}</ref> Macrophages induce "budding" in aggressive human colon cancer subtypes by protease-mediated disruption of tight junctions #MMPMID29731961 Trumpi K ; Frenkel N ; Peters T ; Korthagen NM ; Jongen JMJ ; Raats D ; van Grevenstein H ; Backes Y ; Moons LM ; Lacle MM ; Koster J ; Zwijnenburg D ; Borel Rinkes IHM ; Kranenburg O Oncotarget 2018[Apr]; 9 (28 ): 19490-19507 PMID29731961 show ga Primary human colorectal tumors with a high stromal content have an increased capacity to metastasize. Cancer-associated fibroblasts (CAFs) promote metastasis, but the contribution of other stromal cell types is unclear. Here we searched for additional stromal cell types that contribute to aggressive tumor cell behavior. By making use of the 'immunome compendium'-a collection of gene signatures reflecting the presence of specific immune cell-types-we show that macrophage signatures are most strongly associated with a high CAF content and with poor prognosis in multiple large cohorts of primary tumors and liver metastases. Co-culturing macrophages with patient-derived colonospheres promoted 'budding' of small clusters of tumor cells from the bulk. Immunohistochemistry showed that budding tumor clusters in stroma-rich areas of T1 colorectal carcinomas were surrounded by macrophages. In vitro budding was accompanied by reduced levels of the tight junction protein occludin, but OCLN mRNA levels did not change, nor did markers of epithelial mesenchymal transition. Budding was accompanied by nuclear accumulation of ?-catenin, which was also observed in budding tumor cell clusters in situ. The NF?B inhibitor Sanguinarine resulted in a decrease in MMP7 protein expression and both NF?B inhibitor Sanguinarine and MMP inhibitor Batimastat prevented occludin degradation and budding. We conclude that macrophages contribute to the aggressive nature of stroma-rich colon tumors by promoting an MMP-dependent pathway that operates in parallel to classical EMT and leads to tight junction disruption. äMacrophages induce "budding" in aggressive human colon cancer subtypes(epmc).pdf DeepDyve Pubget Overpricing