Abstract
The product of the nm23 gene was held for a long time to be an important anti-metastatic factor. We found, instead, in a group of well-characterized patients with thyroid carcinomas an increase in nm23 transcripts, the more advanced the tumor stage. These findings could not be accounted for by mutations or amplification of the nm23 gene (1). Our findings were upheld in studies of nm23 protein abundance in thyroid cancer tissues (2). Furthermore, other studies raised doubts about the role of nm23 as an anti-metastasis factor as opposed to its involvement in cell proliferation (3). Because of these considerations we explored the roles of nm23 in fetal development as well as a malignancy-associated factor. We found nm23 not to be particularly highly expressed in invasive tissues e.g. placenta, early in mouse embryonic development. Compared to normal human term placenta cells, the highly metastatic choriocarcinoma cell line JAR expressed much more nm23 (4). Moreover, cytokines known to modulate tumor growth and spread had no influence on JAR nm23 levels (4).
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Shi, Y., Zou, M. & Farid, N.R. The mystery of nm23H1 in thyroid cancer. J Endocrinol Invest 25, 663–664 (2002). https://doi.org/10.1007/BF03345094
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DOI: https://doi.org/10.1007/BF03345094