Stimulation of the growth of metastatic clones of mouse colon adenocarcinoma 26 in vitro by platelet-derived growth factor.

The induction of platelet aggregation by tumor cells was found to be an important determinant for the formation of metastasis of a highly metastatic variant of mouse colon adenocarcinoma 26. We found that the growth of highly metastatic clones, NL-17 and NL-33, of mouse colon 26 was well stimulated by platelet-derived growth factor (PDGF) and the stimulation was dependent on the concentration of the growth factor. The growth of weakly metastatic clones, NL-4 and NL-44, was stimulated marginally by PDGF. Other factors such as transforming growth factor beta and epidermal growth factor did not stimulate the growth of metastatic clones. As the amounts of the receptor of PDGF, as determined by [125I]PDGF binding and mRNA expression, were almost equal in NL-17 and NL-44 clones, the difference in growth potential of these clones after the treatment with PDGF could be explained by post-receptor mechanism(s). The present findings indicate that when tumor cells are arrested in a capillary through the formation of aggregates with platelets, PDGF might play an important role in the establishment of metastasis of mouse colon 26.