Abstract
Two clones isolated from a metastatic variant of mouse colon adenocarcinoma 26; the high metastatic NL-17 and the low metastatic NL-44, induced similar platelet aggregation in vitro. Heterotypic aggregates of tumor cells and platelets were injected i.v. into mice. The lung colonization potential of the NL-17 was dependent on the extent of tumor cell platelet aggregation. This clearly indicates that the interaction of tumor cells with platelets can lead to enhanced tumor metastasis possibly through more efficient intravascular arrest of the heterotypic aggregates. The interaction of tumor cells with platelets could thus be an important determinant for successful metastasis. NL-44, however, did not form pulmonary metastasis even after the tumor cells formed heterotypic aggregates with platelets, suggesting that tumor metastasis, is dependent on the intrinsic nature of tumor cells. Lung extract enhanced the growth of NL-17 more effectively than that of NL-44. These results suggest that, in addition to the interaction of metastatic cells and platelets, host factors including growth-promoting factors might also have an important role in tumor metastasis.
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