Protein found to control tumor growth in certain brea...( This protein was previously thought to ...)

This protein was previously thought to play a role solely in the innate immune system's response to bacterial infection. In the new study, which will be published on-line by the Proceedings of the National Academy of Sciences of the United States of America on January 23, researchers showed for the first time that the protein, which is present in epithelial cells of the intestinal tract and lungs, is linked to the control of malignant cell growth. The study found that over-expression of the protein resulted in the nearly total inhibition of estrogen-dependent tumor growth in mice, and the reduction of estrogen-induced proliferative responses in vitro. In stark contrast, significant tumor growth occurred when Nod1 was absent.

"We have greatly expanded our knowledge of the Nod1 pathway beyond its known role in response to infection," said Richard J. Ulevitch, Ph.D. Ulevitch, who led the study, is a professor and chairman of the Scripps Research Department of Immunology. "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, and will hopefully stimulate researchers to take a fresh look at the Nod1 protein."

In the study, researchers looked at a number of biological processes where Nod1-dependent apoptotic (programmed cell death) pathways were a critical component, including the regulation of tumor cell growth where the failure of malignant cells to undergo cell death led to tumorigenesis. Cells derived from the human breast cancer epithelial cell line MCF-7 the cellular model for estrogen sensitive breast cancer tumors were used to induce tumor growth in severe combined immunodeficiency (SCID) mice. An over-expression of Nod1 in MCF-7 cells resulted in the inhibition of estroge
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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
1-Feb-2006

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