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10.18632/oncotarget.14999 http://scihub22266oqcxt.onion/10.18632/oncotarget.14999 C5362520!5362520 !28178651     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28178651 &cmd=llinks): Failed to open stream: HTTP request failed! 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Stromal fibroblasts present in breast carcinomas promote tumor growth and angiogenesis through adrenomedullin secretion |pdf=|usr=}}{{28178651 }} gab.com Text Stromal fibroblasts present in breast carcinomas promote tumor growth and angiogenesis through adrenomedullin secretion JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28178651 #FOAvip Tumor- or cancer-associated fibroblasts (TAFs or CAFs) are active players in tumorigenesis and exhibit distinct angiogenic and tumorigenic properties. Adrenomedullin (AM), a multifunctional peptide plays an important role in angiogenesis and tumor growth through its receptors calcitonin receptor-like receptor/receptor activity modifying protein-2 and -3 (CLR/RAMP2 and CLR/RAMP3). We show that AM and AM receptors mRNAs are highly expressed in CAFs prepared from invasive breast carcinoma when compared to normal fibroblasts. Immunostaining demonstrates the presence of immunoreactive AM and AM receptors in the CAFs (n = 9). The proliferation of CAFs is decreased by anti-AM antibody (?AM) and anti-AM receptors antibody (?AMR) treatment, suggesting that AM may function as a potent autocrine/paracrine growth factor. Systemic administration of ?AMR reduced neovascularization of in vivo Matrigel plugs containing CAFs as demonstrated by reduced numbers of the vessel structures, suggesting that AM is one of the CAFs-derived factors responsible for endothelial cell-like and pericytes recruitment to built a neovascularization. We show that MCF-7 admixed with CAFs generated tumors of greater volume significantly different from the MCF-7 xenografts in nude mice due in part to the induced angiogenesis. ?AMR and AM22-52 therapies significantly suppressed the growth of CAFs/MCF-7 tumors. Histological examination of tumors treated with AM22-52 and aAMR showed evidence of disruption of tumor vasculature with depletion of vascular endothelial cells, induced apoptosis and decrease of tumor cell proliferation. Our findings highlight the importance of CAFs-derived AM pathway in growth of breast carcinoma and in neovascularization by supplying and amplifying signals that are essential for pathologic angiogenesis. Twit Text FOAVip Stromal fibroblasts present in breast carcinomas promote tumor growth and angiogenesis through adrenomedullin secretion ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28178651 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28178651 #FOAvip English Wikipedia <ref>{{Cite pmid|28178651 }}</ref> Stromal fibroblasts present in breast carcinomas promote tumor growth and angiogenesis through adrenomedullin secretion #MMPMID28178651 Benyahia Z ; Dussault N ; Cayol M ; Sigaud R ; Berenguer-Daizé C ; Delfino C ; Tounsi A ; Garcia S ; Martin PM ; Mabrouk K ; Ouafik L Oncotarget 2017[Feb]; 8 (9 ): 15744-15762 PMID28178651 show ga Tumor- or cancer-associated fibroblasts (TAFs or CAFs) are active players in tumorigenesis and exhibit distinct angiogenic and tumorigenic properties. Adrenomedullin (AM), a multifunctional peptide plays an important role in angiogenesis and tumor growth through its receptors calcitonin receptor-like receptor/receptor activity modifying protein-2 and -3 (CLR/RAMP2 and CLR/RAMP3). We show that AM and AM receptors mRNAs are highly expressed in CAFs prepared from invasive breast carcinoma when compared to normal fibroblasts. Immunostaining demonstrates the presence of immunoreactive AM and AM receptors in the CAFs (n = 9). The proliferation of CAFs is decreased by anti-AM antibody (?AM) and anti-AM receptors antibody (?AMR) treatment, suggesting that AM may function as a potent autocrine/paracrine growth factor. Systemic administration of ?AMR reduced neovascularization of in vivo Matrigel plugs containing CAFs as demonstrated by reduced numbers of the vessel structures, suggesting that AM is one of the CAFs-derived factors responsible for endothelial cell-like and pericytes recruitment to built a neovascularization. We show that MCF-7 admixed with CAFs generated tumors of greater volume significantly different from the MCF-7 xenografts in nude mice due in part to the induced angiogenesis. ?AMR and AM22-52 therapies significantly suppressed the growth of CAFs/MCF-7 tumors. Histological examination of tumors treated with AM22-52 and aAMR showed evidence of disruption of tumor vasculature with depletion of vascular endothelial cells, induced apoptosis and decrease of tumor cell proliferation. Our findings highlight the importance of CAFs-derived AM pathway in growth of breast carcinoma and in neovascularization by supplying and amplifying signals that are essential for pathologic angiogenesis. |Adrenomedullin/genetics/immunology/*metabolism [MESH] |Animals [MESH] |Antibodies, Neutralizing/immunology/pharmacology [MESH] |Blotting, Western [MESH] |Breast Neoplasms/blood supply/genetics/*metabolism [MESH] |Cancer-Associated Fibroblasts/*metabolism [MESH] |Cell Line [MESH] |Cell Proliferation/drug effects/genetics [MESH] |Cells, Cultured [MESH] |Chemokine CXCL12/genetics/metabolism [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |MCF-7 Cells [MESH] |Mice, Inbred C57BL [MESH] |Mice, Nude [MESH] |Neovascularization, Pathologic/*metabolism/pathology/prevention & control [MESH] |Receptors, Adrenomedullin/genetics/immunology/metabolism [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Transplantation, Heterologous [MESH]Stromal fibroblasts present in breast carcinomas promote tumor growth (epmc).pdf DeepDyve Pubget Overpricing