Scientists know that activation of growth factor receptors like epidermal growth factor receptors (EGFR) promote tumor progression in many types of cancer. Now, researchers have shown that EGFR may be shut down with the help of a cytokine known as MIF (macrophage migration inhibitory factor). It's a finding they believe could signal a new way to look at treating tumors. Their study results, which focused on brain, breast, and prostate cancer, are published in the journal Nature Cell Biology.
Exactly how EGFR activation is regulated in the tumor microenvironment has not been understood, nor do human cells have an external antagonist that regulates EGFR. The tumor microenvironment is the cellular landscape in which a tumor exists, including surrounding blood vessels, immune cells, fibroblasts and other cells and structures. It's increasingly being recognized as a key factor in disease progression.
MIF appears to be vital to regulation of EGFR activation in tumor cells' extracellular or external environment. The researchers discovered that modified MIF binds to EGFR. This inhibits EGFR by blocking the epidermal growth factor to bind to EGFR in cancer cells.
The team's findings demonstrate an important mechanism underlying amplified EGFR activation in tumors. This is mediated by downregulation of its antagonist, MIF, in the tumor microenvironment.
According to the researchers, understanding the synergies between EGFR and MIF provide an "instrumental insight" into tumor progression and could open up new approaches to treating cancer by intervening in this self-regulating loop.
Based on material originally posted by University of Texas M. D. Anderson Cancer Center.