Academic Journal
Endothelial Cell Intracellular Ca2+ Concentration Is Increased Upon Breast Tumor Cell Contact and Mediates Tumor Cell Transendothelial Migration
| العنوان: | Endothelial Cell Intracellular Ca2+ Concentration Is Increased Upon Breast Tumor Cell Contact and Mediates Tumor Cell Transendothelial Migration |
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| المؤلفون: | Lewalle, J. M., Cataldo, Didier, Bajou, Khalid, Lambert, C. A., Foidart, Jean-Michel |
| المصدر: | Clinical and Experimental Metastasis, 16 (1), 21-9 (1998-01) |
| بيانات النشر: | Kluwer Academic Publishers |
| سنة النشر: | 1998 |
| المجموعة: | University of Liège: ORBi (Open Repository and Bibliography) |
| مصطلحات موضوعية: | Life sciences, Biochemistry, biophysics & molecular biology, Human health sciences, Oncology, Sciences du vivant, Biochimie, biophysique & biologie moléculaire, Sciences de la santé humaine, Oncologie |
| الوصف: | peer reviewed ; Tumor cell extravasation is a determinant step in the process of hematogenous metastasis. The signal transduction pathways involved in the interactions between tumor cells and the vascular endothelium during transendothelial migration are still undefined. In the present study, we have investigated the influence of human breast adenocarcinoma cells (MCF7) on human umbilical vein endothelial cell (HUVEC) intracellular Ca2+ concentration ([Ca2+]i). We show that the contact between MCF7 cells and a confluent HUVEC monolayer induces an immediate and transient increase in HUVEC [Ca2+]i. This [Ca2+]i rise could not be elicited by tumor cell-conditioned medium, isolated tumor cell membranes, inert beads or normal breast epithelial cells, demonstrating the involvement of specific recognition mechanisms between MCF7 cells and HUVEC. Depletion of HUVEC intracellular Ca2+ stores by the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin as well as the selective depletion of inositol 1,4,5-triphosphate (IP3)-sensitive Ca2+ stores by prior activation of HUVEC using histamine resulted in a complete inhibition of tumor cell-induced [Ca2+]i elevation. Similar results were obtained when HUVEC monolayers were treated with the tyrosine kinase inhibitor herbimycin A, suggesting a role for tyrosine kinase-associated cell surface receptors in tumor cell-endothelial cell interactions. The depletion of HUVEC intracellular Ca2+ stores by thapsigargin was also shown to delay MCF7-induced endothelial cell disjunction, to prevent their spreading on the subendothelial extracellular matrix and transendothelial migration in vitro. These results suggest that transient changes in endothelial [Ca2+]i may govern multiple steps of tumor cell extravasation. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 0262-0898 |
| Relation: | urn:issn:0262-0898; https://orbi.uliege.be/handle/2268/3969; info:hdl:2268/3969; info:pmid:9502074 |
| DOI: | 10.1023/A:1006555800862 |
| الاتاحة: | https://orbi.uliege.be/handle/2268/3969 https://doi.org/10.1023/A:1006555800862 |
| Rights: | restricted access ; http://purl.org/coar/access_right/c_16ec ; info:eu-repo/semantics/restrictedAccess |
| رقم الانضمام: | edsbas.6B5DEB8D |
| قاعدة البيانات: | BASE |
| تدمد: | 02620898 |
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| DOI: | 10.1023/A:1006555800862 |