Meet the badass cancer assassin gene

Illustration for article titled 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.

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Dr Emilio Lizardo

Very good article. p53 is Vital for DNA mismatch repair and removing potentially malignant cells so a p523 problem may contribute to carcinogenesis. However, I must point out that things are always more complicated than reported in the lay press. With very few exceptions, many mutations are required for cancer to develop. The body has several mechanisms to prevent cancer from developing. There is still so much we don't understand but as we comprehend processes on the molecular level better and better we become better at developing drugs to interfere with those processes (targeted therapy) and treat cancer more effectively with fewer side effects. Human beings are just such massively complex systems...

I would also be careful about quoting the cancer stem cell hypothesis. It is gaining a lot of traction right now but I have seen several similar hypothesis - the old two hit model and the instigator/promoter model have both fallen by the wayside as too simplistic. Again, the process is so complex that the hope of finding a single drug that helps all patients with any one cancer, much less all of them, is just a pipe dream.