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Association of the metastatic phenotype with CCN family members among breast and oral cancer cells

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Journal of Cell Communication and Signaling Aims and scope

Abstract

The CCN family of proteins consists of six members with conserved structural features. These proteins play several roles in the physiology and pathology of cells. Among the pathological roles of the CCN family, one of the most important and controversial ones is their role in the expansion and metastasis of cancer. Up to now a number of reports have described the possible role of each CCN family member independently. In this study, we comprehensively analyzed the roles of all six CCN family members in cell growth, migration and invasion of breast cancer cells in vitro and in vivo. As a result, we found the CCN2/CCN3 ratio to be a parameter that is associated with the metastatic phenotype of breast cancer cells that are highly metastatic to the bone. The same analysis with cell lines from oral squamous carcinomas that are not metastatic to the bone further supported our notion. These results suggest the functional significance of the interplay between CCN family members in regulating the phenotype of cancer cells.

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Acknowledgments

This work was supported by the programs Grants-in-Aid for Scientific Research (S)[to M.T.] and (C) [to S.K.] from Japan Society for the Promotion of Science, and by a grant from the program Grants-in-Aid for Exploratory Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan [to M.T.]. Work performed in B. Perbal’s laboratory was funded by French Ministry of Education: EA1556; and by European PROTHETS (Prognosis and Therapeutic Targets of Ewing Family of Tumors, FP6 Contract 503036). We thank Dr. Takanori Eguchi for useful discussions, and Ms. Yoko Tada for valuable secretarial assistance.

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Correspondence to Satoshi Kubota or Masaharu Takigawa.

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Ohgawara, T., Kubota, S., Kawaki, H. et al. Association of the metastatic phenotype with CCN family members among breast and oral cancer cells. J. Cell Commun. Signal. 5, 291–299 (2011). https://doi.org/10.1007/s12079-011-0133-3

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  • DOI: https://doi.org/10.1007/s12079-011-0133-3

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