Being diagnosed with brain cancer comes with a sobering sentence: even with the most aggressive treatments, life expectancy for the most common form of brain cancer—called glioblastoma—is less than two years.
One of the key culprits, many scientists now believe, are cancer stem cells. Cancer stem cells are a subset of cancer cells that have three very unique properties: they can self-renew, they can propagate (or multiply) the cancer, and they can transform into the many types of cells that are found in a tumor.
Cancer stem cells are a relatively new concept, but they have generated a lot of excitement among cancer researchers because they could lead to the design of more effective therapies. And while whether or not they even existed has long been a source of debate among experts, a series of recent research findings have bolstered the notion not only that they exist, but also that they play a significant role in the recurrence of some forms of cancer—including glioblastoma.
Researchers have been identifying, step by step, the many proteins and chemical pathways that form the path from cancer stem cell to tumor. Previous research had found the CDK class of proteins to be present in large quantities in mature cancer cells in patients suffering from glioblastoma. But they suspected something else was at play, helping to keep the CDK proteins switched on in mature cancer cells.
So scientists at McGill University in Canada, led by neurologist Dr. Anita Bellail, dug deeper. In their report, published this week in the journal Nature Communications, the team has pinpointed a new class of proteins at play behind the scenes called SUMO.
Specifically, Bellail and her team observed that the SUMO1 protein in particular modifies a CDK protein called CDK6 in a process the team has dubbed ‘sumylation.’ As Bellail explained in this week’s news release:
“CDK6 sumylation inhibits its degradation and thus stabilizes the CDK6 protein in the cancer.”
In other words, the CDK6 protein does not by itself maintain a presence in the cancer cells. Instead, it requires a little help from SUMO1. As Bellail continued:
“We found that CDK6 sumylation is required for the renewal and growth of the cancer stem cells in glioblastoma.”
It stands to reason, therefore, that shutting off SUMO1 could do the reverse—thus destabilizing CDK6 and, potentially, block the progression of the cancer.
And in further experiments by Bellail and her team, they found exactly that.
These results hold significant promise for finding new ways to treat glioblastoma because now the team has a target: SUMO1. In fact, the research team is now screening for drugs that can target SUMO1 and block it, thus reducing CDK6 levels and, as a result, cancer cells—and one day offering a more optimistic outcome for those diagnosed with glioblastoma.
Want to learn more about cancer stem cells? Check out our 2009 “Spotlight on Cancer Stem Cells” video starring Dr. Michael Clarke, associate director of the Stanford Institute for Stem Cell and Regenerative Medicine.