Meet the badass cancer assassin gene

If the body were a repressive dictatorial regime, one of the enforcers of its brutal conformity would be p53. This is a gene that stalks the body, making sure every cell is kept in check. One of p53's more famous functions is forcing cells with damaged or defective DNA to commit suicide. They can't be allowed to replicate and harm the collective. No doubt p53 would be the bad guy in a post-apocalyptic society, but it's the hero of anatomy. A new scientific study has revealed more about how p53 deals out harsh justice to cells who might spread cancer throughout the body.

Cancer researchers recently discovered how p53 works by studying epithelial cells, the special cells that line the body's organs. These cells are also known for playing host to growing tumors. A tumor on its own is not the biggest worry for cancer researchers. What's worrying is when the cancer starts spreading. And that's why epithelial cells are a big problem - they can turn themselves into mesenchymal cells, which are a kind of adult stem cell that can transform into a variety of other cells. Mesenchymal cells are durable, they can pick up and keep genes that are introduced into them, and they're also highly mobile. So they're easily linked to the spread of cancers from their point of origin to the rest of the body.

If the cells near or on a tumor transform from stationary epithelial to mobile mesenchymal, it could result in the metastasis of the cancer and a significantly worsen the outlook for the patient. So scientists were pleased to see, in a recent set of experiments, that p53 regularly rounds up mesenchymal cells and makes them transform back into epithelial cells. When cells begin to go mesenchymal, p53 starts a process that blocks two proteins that allow the transformation and forces the cell back into its previous submissive state.

The evidence for this process is strong. Scientists conducted a series of experiments showing that activity of p53 put a stop to epithelials trying to go mesenchymal. But hobbling the activity of p53 encouraged cells to go mesenchymal. When scientists studied breast tumor tissues, low levels of p53 matched up with high levels of epithelial-to-mesenchymal transformation.

Low or mutated p53 are present in many cancer types, and low levels of the gene mean a poor prognosis. Finding some way to boost expression of p53, or introducing some drug or therapy that fills in for the gene might be a very good way to contain cancer and prevent metastasis. No one acts out on p53's watch.

Via The International Society for Stem Cell Research and Nature Cell Biology.