"Equally exciting, we show that this mechanism involves a fundamental receptor of the immune system, TLR8, suggesting that the implications of this discovery may extend to other diseases such as autoimmune and inflammatory diseases," Fabbri says.Key findings of the study include the following:
In human macrophages, microRNA-29a and microRNA-21 bind with TLR8, causing the macrophages to secrete tumor-necrosis-factor alpha and interleukin-6, two cytokines that promote inflammation.
Increased levels of the two cytokines were associated with an increase in the number of tumors per lung in an animal model, while a drop in those levels led to a drop in the number per lung, suggesting that they also play a role in metastasis.Funding from the NIH/National Cancer Institute (grants CA150297, CA135030, CA124541, and CA148302) and a 2009 Kimmel Foundation Fellowship supported this research.
Darrell E. Ward | EurekAlert!
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