UC Berkeley researchers have discovered a method of reducing cancer-cell aggression and impairing the ability of cancer cells to form tumors, which may have major implications for the future of cancer treatment, according to a study published Monday.
In the study, researchers discovered that inhibiting a single enzyme could significantly reduce cancer and tumor growth. The finding resulted from an analysis of the role of ether lipids — a kind of lipid that appears in high concentration in human cancers — in the development of cancer.
To gauge what effect ether lipids have on the reproduction of cancer cells, the research team targeted the enzyme that is critical in the creation of the lipids. Once the enzyme, AGPS, was disabled, fewer ether lipids were created. Also, the team found, reducing the abundance of ether lipids slowed the rate of cancer and tumor growth.
“(The researchers) have made the important observations that disrupting ether lipid synthesis in cancer cells impairs their ability to divide, makes them less likely to spread around the body and inhibits signaling within the cancer cell,” said David Russell, editor of the study and vice provost and dean of basic research at UT Southwestern Medical Center.
Scientists have known about the presence of ether lipids in cancer cells for decades, but the study suggests a significance in the correlation. By studying the effect that the removal of AGPS has on cancers and tumors, researchers realized that ether lipids play a significant role in their growth.
“We didn’t know what we would find, because no one knew why these cancer cells have a high number of ether lipids, so we followed this,” said Daniel Nomura, the study’s principal investigator and an assistant professor in UC Berkeley’s department of nutritional science and toxicology.
In experiments, mice were injected with cancer cells. Those for which AGPS was disabled had no tumor growth, but the mice in the control group quickly developed tumors.
Many scientists and researchers with knowledge of the study consider its findings encouraging because of their potential applications in clinical cancer treatment.
“We are currently working to develop a small molecule inhibitor of this gene that may someday be used, in combination with current chemotherapeutic agents, as an effective cancer treatment,” said Daniel Benjamin, the study’s lead author and a doctoral student in the Nomura Research Group.
But Nomura said that before a clinical version of the chemical inhibitor can be created, many more studies need to be conducted. In particular, more information needs to be gathered on how lipids operate within cancer cells, as well as whether the method would yield similar results in humans.
