BRAF kinase is mutated, typically val 600 --> glu (v600E) to induce wide spectrum of cancers. MAPK signaling pathway is essential for tumorigenesis, in which a chain of proteins in the cell that communicate a signal from a receptor on the surface of cell to the DNA in the nucleus of the cell. Phosphorylation of MEK1/2 by BRAF is one among the steps in pathway. By the way, phosphorylated MEK1/2 in turn phosphorylates ERK1/2. In normal cells MAPK pathway is turned off shortly but incase of any mutation it cannot be turned off and leads to uncontrolled proliferation that results in tumorigenesis. Mutated BRAF (BRAF Ｖ600E) along with a conjugate, Cu-MEK1, enhance ERK1/2 phosphorylation which results in tumor growth. MEK1 has great affinity towards copper. So, when it binds to copper, results in high level of P-ERK1/2 (phosphorylated ERK1/2) which further enhance tumor formation. Hence it is essential to suppress copper influx inside the cell. Ctr1 (copper transportor 1) is responsible of transporting copper inside the cell. It is believed that if ctr1 is suppressed which may result in copper deficiency there by MEK1 cannot make conjugate with copper and cannot enhance tumor growth.
Reference: http://www.nature.com/nature/journal/v509/n7501/full/nature13180.html
