Prostaglandin E2 receptor modulation affects tumor cell adhesion to laminin

✍ Scribed by Shao-Zeng Zhang; Amy M. Fulton

• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 689 KB
• Volume: 149
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041490206

✦ Synopsis

We have shown previously that murine mammary adenocarcinoma cells both synthesize prostaglandin E, (PGE,) and have a high affinity receptor for this ligand.

Modulation of either PGE synthesis or PGE receptor function changes the metastatic potential of these cells. Because of the importance of laminin and laminin receptors to the metastatic process, we asked whether or not the PCE receptor participates in tumor cell-laminin interactions. As has been reported for many other tumor cells, laminin and the laminin-derived peptide PA22-2, containing the sequence IKVAV, mediate attachment of line 410.4 mammary tumor cells in vitro. We now demonstrate that the attachment of 41 0.4 cells to laminin or peptide PA22-2 was significantly inhibited by three PCE receptor antagonists, LEO1 01, SC19220, and sodium meclofenamate. LEO101 was most active, inhibiting tumor cell adhesion in a dose-dependent manner in the absence of nonspecific toxicity. These receptor antagonists had no effect on the PA22-2mediated attachment of a PGE receptor negative tumor cell line, except at the highest concentration of LEO101 tested. No inhibition of adhesion to Type I collagen was seen. These results indicate that the PCE, receptor modulates tumor cell adhesion to laminin which may subsequently affect the in vivo process of metastasis.

Methods

Tumor cells Tumor cell lines 410.4 and 168 were derived from a single spontaneously arising mammary adenocarcinoma of a BALBlcfC3H mouse (Miller et al., 1983).