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An enzyme that cancer cells eliminate, apparently so they can keep proliferating, may hold clues to more targeted, effective cancer treatment, scientists say.
In a high-stakes tit for tat, protein kinase G enables healthy cells to stay on task to proliferate, differentiate then provide a useful function. Cancer somehow reduces or eliminates PKG and cells get stuck proliferating.
“The bottom line is, in normal tissue, you can see PKG being expressed; but tumors or cell lines that correlate with those tissues don’t have nearly as much,” says Dr. Darren Browning, cancer researcher at the Medical College of Georgia.
Cell lines used for all types of research appear to support his hypothesis. Many are actually cancer cells because of their proclivity to keep producing; Dr. Browning and others have shown PKG is lost in these cells. “You split them once or twice and they kind of lose their character,” he says.
The same appears true for tumors in people, says Dr. Browning, whose lab has found dramatic differences in PKG levels in tumors compared to even nearby, healthy tissue removed in surgery to ensure a cancer-free margin.
The findings made him wonder if the change in PKG level was just an artifact or was critical to cancer survival. “A lot of proteins are lost by cancer cells, so we asked, ‘What happens if we put PKG back into the cancer cells?'”
He took metastatic colon cancer cells, created a system for reintroducing PKG, then put the cells into mice without an immune system. He admits he was disappointed that the PKG-enhanced cells grew but became very interested in how they grew.
Cancer cells without PKG created hard, solid tumors that spread. PKG-enhanced cells created a soft, non-invasive tumor that literally fell apart on contact and seemed to grow in little islands. After consultation with pathologists and others, he realized the PKG-enhanced cells were congregating around the few blood vessels. “We know that cancer cells, particularly colon cancer cells, are very aggressive at bringing blood vessels into the tumor,” he says. Cells poor at recruiting blood vessels don’t grow well, which seems to be the case for PKG-enhanced colon cancer cells.
Now he wants to know how PKG nullifies aggressive metastatic cancer cells. “We think PKG inhibits cancer by getting rid of a cancer-promoting gene called beta-catenin, which slows growth and blocks the tumor’s ability to recruit blood vessels that are needed to grow bigger,” says Dr. Browning, who recently received a $720,000 American Cancer Society grant to pursue his hypothesis. His proposal was ranked number one by the ACS Cell Structure and Metastasis Study Section.
