| Effects of tumor cell-derived interleukin 1 alpha on invasiveness of metastatic clones of murine RCT sarcoma through endothelial cells. | |
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MedLine Citation:
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PMID: 10050109 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Interleukin 1 alpha (IL-1alpha) production and invasiveness through mouse lung endothelial cells (MLE) were investigated in high-metastatic RCT+ and low-metastatic RCT- clones established from poorly differentiated murine sarcoma. Apparently, a higher level of IL-1alpha was derived from RCT+ cells than from RCT- cells. In an invasion assay, the number of cells which penetrated the MLE monolayer in RCT+ was significantly greater than that in RCT-. The invasiveness of RCT+ and RCT- cells was stimulated by additional recombinant mouse IL-1alpha (rIL-1alpha) in a dose-dependent manner. Anti-mouse IL-1alpha monoclonal antibody (anti-IL-1alpha mAb) significantly inhibited the invasiveness of RCT+ and RCT- cells through the MLE monolayer. However, in RCT+ cells these effects were higher than in RCT- cells. In an attachment assay, the ability of RCT+ cells to attach to the MLE monolayer was significantly higher than that of RCT- cells. The attachment ability of RCT+ and RCT- cells to the MLE monolayer was significantly increased by the pretreatment with rIL-1alpha in a dose-dependent manner. In a retraction assay, conditioned medium of RCT+ stimulated the retraction of the MLE monolayer more markedly in comparison with conditioned medium of RCT-. The retraction of the MLE monolayer was stimulated by additional rIL-1alpha in a dose-dependent manner. The increased retraction of the MLE monolayer was closely associated with the enhancement in tumor cell invasiveness. These findings suggest that IL-1alpha derived from RCT+ and RCT- cells might contribute to the enhancement of tumor cell invasion by stimulating the attachment to the MLE monolayer and retraction of the MLE monolayer. |
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Authors:
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T Yasuda; H Matsui; M Kanamori; K Yudoh; K Ohmori; M Aoki; H Tsuji |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine Volume: 20 ISSN: 1010-4283 ISO Abbreviation: Tumour Biol. Publication Date: 1999 Mar-Apr |
Date Detail:
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Created Date: 1999-04-20 Completed Date: 1999-04-20 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8409922 Medline TA: Tumour Biol Country: SWITZERLAND |
Other Details:
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Languages: eng Pagination: 105-16 Citation Subset: IM |
Affiliation:
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Department of Orthopedic Surgery, Toyama Medical and Pharmaceutical University, Toyama, Japan. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibodies, Monoclonal / pharmacology Cell Adhesion / drug effects Cell Line Clone Cells / cytology, drug effects, metabolism Coculture Techniques Culture Media, Conditioned / pharmacology Dose-Response Relationship, Drug Endothelium, Vascular / cytology* Interleukin-1 / immunology, metabolism, physiology* Male Mice Mice, Inbred C3H Neoplasm Invasiveness / immunology* Sarcoma, Experimental / metabolism*, pathology Specific Pathogen-Free Organisms Tumor Cells, Cultured |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Monoclonal; 0/Culture Media, Conditioned; 0/Interleukin-1 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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