Scientists at the University of California, San Diego School of Medicine claim that they have identified a protein produced that enhances the spread of lung cancer by stimulating the activity of inflammatory cells.
The researchers said, “Their work may be helpful in gaining a deeper understanding as to how advanced cancer cells usurp components of the host innate immune system to generate an inflammatory microenvironment hospitable for the metastatic spread of lung cancer. That, in turn, could result in a therapy to limit metastasis of lung cancer”.
Lead researcher Michael Karin, UC San Diego Distinguished Professor of Pharmacology and Pathology said, “His team used a straightforward biochemical approach to identify proteins produced by metastatic cancer cells, which are responsible for generation of an inflammatory microenvironment that supports the growth of metastases.”
He further added, “The team focused on macrophages, white blood cells that are key players in the immune response to foreign invaders as well as in cancer growth and progression, and screened for factors produced by metastatic cancer cells in mice that could stimulate the activity of this inflammatory cell type.”
The researchers said, “Biochemical purification of proteins secreted by LLC cells resulted in identification of an extra cellular matrix protein called versican as the major macrophage activator and metastasis enhancing factor.”
They found that versican strongly enhances LLC metastatic growth by activating receptors that lead to production of cytokines - signalling proteins that regulate the immune system. One of those receptors, TLR2, and a cytokine, TNFa, were found to be required for LLC metastasis.
However, the normal function of TLR2 and TNFa is in host defence-innate immunity to microbial infections. Karin said that his team's findings were relevant, not just to the mouse model, but also to human lung cancer - the most common cause of cancer-related deaths worldwide.
