Mechanisms of colon cancer binding to substratum and cells
- 56 Downloads
Binding of colon cancer to extracellular matrix (ECM) proteins and mesenchymal cells that comprise the basement membrane is important in migration and metastasis. This study defines the conditions and surface structures necessary for adhesion of HT-29 cells to ECM proteins and cell monolayers. Binding began within minutes and peaked by 1 hr, with 80–95% of HT-29 cells binding to the ECM proteins, collagen IV, laminin, fibronectin, and vitronectin and 40–75% binding to monolayers of fibroblasts, smooth muscle cells, and HT-29 cells. Treating mesenchymal cells with the fibrogenic cytokines, IL-1, IL-4, or TNF-α, which increase production of ECM proteins, did not alter binding of HT-29 cells to these monolayers. Attachment of HT-29 cells to cell monolayers was inhibited by cytochalasin D and sodium azide, but not cycloheximide or neuraminidase. Attachment to ECM proteins, in contrast, was unaffected by any of these metabolic inhibitors but required certain divalent cations (Mg2+ and Mn2+ but not Ca2+). Antibody to the integrinβ1 chain (CD29) eliminated binding to collagen and laminin but not to fibronectin, fibroblasts, and HT-29 monolayers. Antibody to the vitronectin receptor inhibited binding to fibronectin. Antibodies to integrinα1–α6 chains had no effect on any adhesion event. Three colon cancer cell lines were tested for expression of VLA antigens:α2 andα3 were detected on all three,α1 andα6 were variably expressed, whileα4 andα5 were absent. This study demonstrates that several mechanisms account for tumor cell attachment to substratum and cells.
Key wordscolon cancer very late activation extracellular matrix collagen laminin fibronectin
Unable to display preview. Download preview PDF.
- 1.Nigam AK, Pignatelli M, Boulos PB: Current concepts in metastasis. Gut 35:996–1000, 1993Google Scholar
- 3.Pignatelli M, Smith MEF, Bodmer WF: Low expression of collagen receptors in moderate and poorly differentiated colorectal adenocarcinomas. Br J Cancer 61:636–638, 1989Google Scholar