How destroying a tumor promoter could lead to new cancer treatments
Scientists have cracked a cell mechanism that drives tumor formation in most types of cancer. This finding could lead to much-needed new therapies for cancer, including the hard-to-treat triple-negative breast cancer.
The discovery concerns the molecular activity of the tumor suppressor protein p53. This protein sits inside the nucleus of the cell and protects the cell's DNA from stress. It has acquired the nickname "guardian of the genome" for this reason.
However, mutated forms of p53, which are common in cancer, behave differently than regular p53. Instead of protecting the cell, they can take on oncogenic, or tumor-promoting, properties and become active drivers of cancer.
Previous studies had already shown that p53 mutations are more stable than their nonmutant counterparts and can accumulate until they eclipse them in the nucleus. However, the mechanism behind the stability of p53 mutations remained unclear.
Now, researchers from the School of Medicine and Public Health at the University of Wisconsin-Madison have unpicked the stabilizing mechanism, and they suggest that it offers a promising target for new cancer treatments. Their findings feature in the journal Nature Cell Biology.
The stabilizing process involves two molecules: the enzyme PIPK1-alpha and its "lipid messenger" PIP2. Between them, they appear to regulate the function of p53.
"Although p53 is one of the most commonly mutated genes in cancer," says co-lead researcher and study author Vincent L. Cryns, who is a professor of medicine, "we still do not have any drugs that specifically target p53."
