Peritoneal carcinomatosis involves a series of events including
tumor cell interactions with mesothelial cells and the extracellular matrix (ECM). We have studied the adhesive and invasive properties of four human
colorectal carcinoma cell lines (Co115, HT29, SW480, SW620) confronted in vitro with a human mesothelial cell monolayer or with the ECM
proteins collagen IV,
laminin-1,
fibronectin,
tenascin-C and
vitronectin. Quantitation was achieved following staining of
tumor cells with the
calcein-AM fluorescent dye. We found that all four cell lines rapidly adhered to a mesothelial cell monolayer. This adhesion event was not inhibitable by anti-
integrin and anti-CD44
antibodies. Following initial attachment, the SW480 and SW620 cells invaded the mesothelial cell monolayer more aggressively than HT29 and Co115 cells. All cell lines adhered to ECM
proteins with each one exhibiting an individual adhesion pattern. Adhesion to matrix was completely
integrin-dependent. When tested in an invasion assay, HT29 and Co115 cells crossed
Matrigel-coated filters while SW480 and SW620 cells did not. This invasion was inhibited by anti-beta 1
integrin antibodies. Taken together, our results demonstrate that the initial
colorectal tumor cell-mesothelial cell interaction occurs through an
integrin-independent mechanism while adhesion to matrix
proteins and invasion through
Matrigel are
integrin-dependent events. Furthermore, the different invasive capacity of SW480 and SW620 versus HT29 and Co115 cells upon interaction with a mesothelial cell monolayer or
Matrigel suggests that these two invasion events may be mediated by distinct mechanisms.