ArticleClinical & experimental metastasis1998
Endothelial cell intracellular Ca2+ concentration is increased upon breast tumor cell contact and mediates tumor cell transendothelial migration.
Article in Clinical & experimental metastasis, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Long-range gap junctional signaling controls oncogene-mediated tumorigenesis in Xenopus laevis embryos.Frontiers in physiology · 2014Article
- TMEM16A alternative splicing coordination in breast cancer.Molecular cancer · 2013Article
- Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters.World journal of biological chemistry · 2012Article
- The role of connexins in prostate cancer promotion and progression.Nature reviews. Urology · 2012Review
- Tissue inhibitor of metalloproteinase-2 regulates matrix metalloproteinase-2-mediated endothelial barrier dysfunction and breast cancer cell transmigration through lung microvascular endothelial cells.Molecular cancer research : MCR · 2010Article
- Mesenchymal stem cells as therapeutic tools and gene carriers in liver fibrosis and hepatocellular carcinoma.Gene therapy · 2010Review
- Molecular mechanisms of metastasis in prostate cancer.Asian journal of andrology · 2009Review
- Calcium signaling and T-type calcium channels in cancer cell cycling.World journal of gastroenterology · 2008Review
- The stage-specific function of gap junctions during tumourigenesis.Cellular & molecular biology letters · 2008Review
- Increased expression of connexins 26 and 43 in lymph node metastases of breast cancer.Journal of clinical pathology · 2006Article
- Involvement of phospholipase C signaling in melanoma cell-induced endothelial junction disassembly.Frontiers in bioscience : a journal and virtual library · 2005Article
- Invasive characteristics of human prostatic epithelial cells: understanding the metastatic process.British journal of cancer · 2005Article
- Connexin 43 mediated gap junctional communication enhances breast tumor cell diapedesis in culture.Breast cancer research : BCR · 2005Article
- MUC1 mediates transendothelial migration in vitro by ligating endothelial cell ICAM-1.Clinical & experimental metastasis · 2005Article
- A modified Boyden chamber assay for tumor cell transendothelial migration in vitro.Clinical & experimental metastasis · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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