Nod1 Protein Controls Estrogen-Sensitive Tumors

For an in vitro model they used cultures of the human breast cancer epithelial cell line MCF-7. In vivo studies were carried out on mice with severe combined immune deficiency (SCID).

Results published in the January 30, 2006, online edition of the Proceedings of the [U.S.] National Academy of Sciences revealed that in MCF-7 cells, the absence of Nod1 correlated with tumor growth, increased sensitivity to estrogen-induced cell proliferation, and failure to undergo Nod1-dependent apoptosis. In contrast, overexpression of Nod1 in MCF-7 cells resulted in inhibition of estrogen-dependent tumor growth and reduction of estrogen-induced proliferative responses.

A similar response to the activity of Nod1 was seen in the mouse model. Over-expression largely abolished estrogen-dependent tumor growth. Even implantation of estrogen pellets failed to stimulate tumor growth. When Nod1 was absent, however, the tumors grew and killed the mice.

"We have greatly expanded our knowledge of the Nod1 pathway beyond its known role in response to infection,” said senior author Dr. Richard J. Ulevitch, professor of immunology at Scripps Research Institute. "These unexpected findings offer the first real evidence that this pathway may regulate tumor growth and suggest a potentially new mechanism for controlling this type of breast cancer. Unraveling the intricate mechanisms of this previously unknown pathway opens up the potential for future development of novel therapeutics.”



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