Ultimately, unlocking the role of MICAL-2 may open the door to an entirely new kind of metastatic cancer drug. "We now know that drugs that target MICAL-2 exhibit beneficial effects in preclinical tests of metastasis," Dr. The finding is important because it shows that MICAL-2 is a viable drug target and that if it is blocked, cancer metastasis can be halted. Jaffrey's team demonstrated that the new drug, known as CCG-1423, worked by blocking MICAL-2.
Working with these investigators, who are co-authors on the Cell paper, Dr. While the Weill Cornell scientists were investigating the role of MICAL-2 in the SRF signaling pathway, they realized that colleagues at the University of Michigan were developing a new drug that stopped cancer cell metastasis, though the Michigan investigators did not know how their drug worked. These cancers were also much more likely to spread to other parts of the body, which supports the idea that MICAL-2 may act as a switch that causes cancer cells to metastasize.īecause of their structure, enzymes like MICAL-2 are typically good targets for drug therapies. Jaffrey's lab did an analysis of genetic data from a number of different cancer types, they found that many of the most deadly tumors had high levels of MICAL-2. "We think that this upregulation of MICAL-2 is causing them to be metastatic." "One of the things we're finding that we're really excited by is that there are many cancers, especially metastatic cancers that have the poorest prognosis, that also have very high levels of MICAL-2," Dr. MICAL-2, it turned out, triggered the activity of SRF, reprogramming the transcription in the cells to resemble that seen in metastatic cells. Lundquist examined these cells, he found that SRF had become overactive. (Unregulated cell growth is the fundamental cause of cancer.) When Dr. Jaffrey's lab, found that cells expressing MICAL-2 resembled cancer cells in their shape and high growth rate. Mark Lundquist, a postdoctoral associate in Dr. Samie Jaffrey, a professor of pharmacology, discovered that an enzyme known as MICAL-2 is necessary for SRF to function in cells. Investigators in the laboratory of senior author Dr. The protein plays a critical role in the life cycle of cells, regulating their growth and controlling their ability to migrate through tissue, a critical step in the process of metastasis. SRF is a transcription factor, meaning that it binds to specific DNA sequences and controls the expression of messenger RNA in a process known as transcription. 16 online edition of Cell, centers on a protein known as serum response factor (SRF). This image shows how MICAL-2 reorganizes actin in the nucleus, which leads to the activation of the SRF transcription factor. The SRF pathway is known to be important for the invasion of cancer cells into normal tissue - the process of cancer spread and metastasis.
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