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[Cancer Research 48, 5129-5132, September 15, 1988]
© 1988 American Association for Cancer Research

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Metastatic Capacity and Intercellular Communication between Normal Cells and Metastatic Cell Clones Derived from a Rat Mammary Carcinoma1

Jun-ichi Hamada2, Noritoshi Takeichi and Hiroshi Kobayashi

Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Sapporo 060, Japan

Three highly metastatic clones and two weakly metastatic clones were obtained from a spontaneously arising mammary carcinoma in an SHR rat. The difference in their capacity to generate metastatic ability was recognized when the tumor cells were implanted s.c. but not when they were implanted i.v. This evidence possibly indicates that the difference in the metastatic capacity of these clones is caused by different potential for detachment from the primary site and for intravasation during the various steps of metastasis.

There are no differences between highly and weakly metastatic clones with regard to their in vitro growth characteristics (doubling time, saturation density, plating efficiency, etc.), homotypic aggregation, and adhesiveness to plastic matrices and fibroblast monolayers. Therefore, we used a dye transfer method to examine the relationship between the metastatic capacity of tumor cells and the capacity of tumor cells to make junctional communication with normal fibroblasts. We found that the incidence of intercellular communication between weakly metastatic clone cells and fibroblasts (derived from normal s.c. tissues and tumor tissues) was significantly higher than that between highly metastatic clone cells and fibroblasts.

These results suggest that junctional communication between tumor cells and normal fibroblasts may play a part in the early stage of cancer metastasis.

1 This work was supported by a Grant-in-Aid for Cancer Research from the Japanese Ministry of Education, Science and Culture.

2 To whom requests for reprints should be addressed.

Received 4/28/87. Revised 5/24/88. Accepted 6/ 6/88.




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Copyright © 1988 by the American Association for Cancer Research.