14 DAY TRIAL // A team of researchers in the United States announces a groundbreaking discovery in prostate cancer research. The investigators argue that a protein regularly involved in the self-renewal of normal prostate stem cells also plays a role in promoting the morphing of normal cells into cancer cells.
The finding is very worrying because oncologists relied on these proteins to help repair injured cells and tissue, that were affected by hormone-withdrawal therapies commonly used to combat cancer.
However, this turns out not to be the case, say investigators at the University of California in Los Angeles (UCLA) Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research.
They believe that the new discovery could be used for controlling both cancer growth and progression. Details of the work appear in the December 2 early online issue of the esteemed journal Cell Stem Cell.
The investigation itself was conducted in primary cells, and on unsuspecting animal models, the team says, but plans are to move to human experiments as soon as possible.
Bmi-1, the protein analyzed in the study, has often been observed to be over-expressed and up-regulated in patients suffering from prostate cancer. But its exact role and function in the body had yet to be discovered.
According to Dr. Owen Witte, the senior author of the study and the director of the Broad Stem Cell Research Center, the proteins is important for the self-renewal activity and maintenance of prostate stem cells that have highly proliferative abilities.
If the protein's expression is blocked, then self-renewal is stopped, adds Witte, who is also a Howard Hughes Medical Institute investigator.
Furthermore, the inhibition also stops the spread of cancer in animal models that lack the PTEN gene, a famous suppressor of tumor formation. Organisms lacking it experience a rampant spread of cancer.
“We conclude by these results that Bmi-1 is a crucial regulator of self-renewal in adult prostate cells and plays important roles in prostate cancer initiation and progression,” Witte explains.
“It was encouraging to see that inhibiting this protein slows the growth of even a very aggressive prostate cancer, because that could give us new ways to attack this disease,” he adds.
“Prostate cancer can be initiated by so many different mutations, if we can find a key regulator of self-renewal, we can partially control the growth of the cancer, no matter what the mutation is,” says research scientist Rita Lukacs.
“We're attacking the process that allows the cancer cells to grow indefinitely. This provides us an alternate way of attacking the cancer by going to the core mechanism for cancer cell self-renewal and proliferation,” she adds.
Lukacs is the first author of the new research paper, and also a PhD student in Witte's lab at UCLA. Funding for the new work came, among others, from the California Institute for Regenerative Medicine (CIRM) and the Howard Hughes Medical Institute.