Targeting Mitochondrial Metabolism in Triple-Negative Breast Cancer
Posted: Tuesday, June 11, 2019
Marsha Rich Rosner, PhD, of the University of Chicago, and colleagues have focused research efforts on enhancing the efficacy of inhibitors of mitochondrial metabolism through restricting metabolic plasticity. They hope to find an effective treatment of triple-negative breast cancer, as well as other tumor types that use the BACH1 gene or other key regulators of mitochondrial metabolism. In fact, a potential combination therapeutic strategy, based on their research findings published in Nature, centers on two agents commonly used for other purposes.
“We think we may have found a way to treat resistant breast cancers that currently have no targeted therapy by repurposing two older drugs, metformin and heme [also known as panhematin or hemin], that are already in the marketplace,” said Dr. Rosner in a University of Chicago press release.
The researchers studied whether manipulating metabolic pathways could increase the efficacy of cancer treatments that target mitochondrial metabolism. They looked at using BNB and CNC homology1 (BACH1) to target mitochondrial metabolism.
“When cancer cells are treated with hemin, BACH1 is reduced, causing BACH1-depleted cancer cells to change metabolic pathways,” explained coauthor Jiyoung Lee, PhD, an instructor affiliated with Dr. Rosner’s laboratory. This process, through the use of the combination of hemin plus metformin, “can suppress tumor growth, and we validated this in mouse tumor models,” he added.
“To our knowledge,” the investigators concluded, “the role of BACH1 as a novel regulator of metabolism has not previously been recognized or studied.”
Disclosure: The study authors reported no conflicts of interest.
