The cure to cancer may lie close to home and it might come in the form of a biological assassin.
Siva Kolluri, assistant professor of cancer biology in the environmental and molecular toxicology department at Oregon State University, discovered a cancer-killing molecule nearly nine years ago and published an article last fall that revealed his team’s findings on how to enact the killer.
Although it was years in the making, Kolluri and his team’s discovery was a surprise even to them, when Kolluri first realized that the dangerous force of a cancer-protecting protein could not only be neutralized, but also turned cancer-killing.
“We said, ‘We have something new here. We cannot ignore this; this is working,’” he said. “Thousands of scientists across the world have studied this protein for years.”
After publishing their initial findings in some of the nation’s top science journals, Kolluri’s team pursued the research further. At the top of Kolluri’s agenda for the past several years has been finding a way to force the cancer cell’s protector, the protein Bcl-2, into acting as a cancer killer.
Now, he and a team of researchers from OSU and Burnham Institute for Medical Research in La Jolla, Calif., have developed a peptide that invokes the Bcl-2 cancer-killing capabilities and presented their findings in the medical science journal Cancer Cell last fall.
While scientists knew that Bcl-2 could either protect or destroy cancer cells, they didn’t previously know how to induce the protein’s destructive capability. Kolluri identified a molecule that would do the job.
What Kolluri and his colleagues noticed “accidentally” in lab research those years ago became the foundation for a groundbreaking study, which led them to develop a peptide that could revolutionize how certain cancers are treated.
Kolluri and other researchers found that nuclear receptor Nur77 can interact with and convert Bcl-2 cells, which protect cancer cells and allow tumors to resist treatment and continue growing, into cancer cell killers.
Hui Zong, a University of Oregon assistant professor of biology and cancer biology researcher, said the discovery is innovative.
“Bcl-2 is a molecule that protects the (cancer) cell from dying,” Zong said. “If they can turn Bcl-2 into a pro-death cell, that will be interesting to help cure cancer.”
The same protein that protects cancer cells appears in many types of cancer, Kolluri said in a statement, and is responsible for cancer cells’ resistance to many chemotherapeutic drugs and radiation. For that reason, cancer-fighting drugs that target Bcl-2 are an appealing possibility.
In an OSU press release, Linda Wolff, a leukemia researcher at the National Institutes of Health’s Center for Cancer Research in Bethesda, Md., said the researchers’ discovery is “rare” in the world of cancer research.
“Although the peptide they studied causes cancer cells to die, its effect on normal cells seems to be quite minimal,” she said. “A big problem in cancer research has been getting therapies that don’t kill normal cells.”
Zong said the new research could lead to much-improved cancer treatments, since it would attack the cancer in an unprecedented way.
“It’s a novel idea; nobody’s done this before,” he said. “Most treatments are actively dividing cells, and that’s how they are killed.”
Dividing cells causes the common negative side effects of chemotherapy treatment, such as hair loss and damage to the intestinal lining. The prospect of targeting Bcl-2 cells could treat cancer in a new way sans cell division and the common side effects.
Bcl-2 is expressed in the cancer cells of many types of cancer. However, Kolluri said, the peptide has not killed cancer cells where the protein is not present.
“We’ve tried it on mice and found that if you do not have Bcl-2, the cancer does not respond at all,” he said.
While Kolluri and his colleagues have high hopes that the discovery will lead to effective therapeutic cancer treatments, they still face the challenge of isolating the Bcl-2 cells for conversion in clinical studies.
“This was years of work, commitment and belief,” Kolluri said. “It was a collaborative effort.”
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