The protein that keeps cancer cells alive

Researchers from the Walter and Eliza Hall Institute have discovered a protein that is key to the development of blood cancers caused by a common genetic error.

Around 70% of human cancers have abnormally high levels of the protein MYC, which forces cells into unusually rapid growth. Writing in the journal Cell Reports, the scientists revealed that blood cancers driven by MYC could be prevented by lowering the levels of another protein, called MCL-1.

Study co-author Dr Stephanie Grabow said developing cancer cells are dependent on MCL-1, a protein that keeps stressed cells alive by preventing programmed cell death (apoptosis). “No-one had realised just how vulnerable cells undergoing cancerous changes are to a relatively minor reduction in the levels of MCL-1,” she said. “We found that MCL-1 is critical for keeping developing cancer cells alive through the stressful events that cause the transformation of a healthy cell into a cancerous cell.

“This result is particularly exciting because MCL-1 inhibitors are already in development as anticancer drugs. Our colleagues had previously discovered that reducing the activity of MCL-1 is a promising strategy to treat malignant MYC-driven cancers. We have now shown that the same approach might be able to prevent those cancers from forming in the first place.”

Co-author Dr Brandon Aubrey added that the research could inform future strategies to prevent cancer, stating, “Cancer researchers are building a better picture of who is at risk of developing cancer and enhancing how we can detect early-stage cancer in people before it has grown to the point of causing illness.

“Our research has suggested that dependency on MCL-1 could be a key vulnerability of many developing cancers,” he said. “In the future, MCL-1 inhibitors might have potential benefit for treating the very early stages of MYC-driven cancers, or we may even be able to use these agents to prevent people from getting cancer in the first place.”

Originally published here.