By Mariel Emrich, Columbia Grammar and Preparatory School
Researchers at the Kimmel Cancer Center at Jefferson have identified cancer cell mitochondria as the energy provider of tumor growth. This will allow room for new therapeutic targets in breast cancer.
In the online December 1st issue of Cell Cycle, Michael P. Lisanti, professor and chair of Stem Cell Biology and Regenerative Medicine at Thomas Jefferson University, and colleagues reported the first evidence that breast cancer cells perform enhanced mitochondrial oxidative phyosphyorylation (OXPHOS) to produce high amounts of energy. This could be extremely advantageous in the development of new cancer protocols because the treatments for breast cancer may change due to the discovery of the specific energy source used in the reproduction of cancer cells.
Over the past 85 years, it has been debated whether the energy cancer cells require to grow comes from mitochondria or whether it comes exclusively from glycolysis (known as the 'Warburg Effect'.) However, the researchers at the Kimmel Cancer Center at Jefferson have shown that glycolysis (a relatively inefficient method of producing energy) takes place in the surrounding stromal cells, rather then in epithelial cancer cells.
The researchers, including co-author and collaborator Federica Sotgia, assistant professor in the Department of Cancer Biology, looked at mitochondrial function using COX activity staining in human breast cancer samples to study mitochondria’s role directly. Researchers found that human breast cancer epithelial cells showed high levels of mitochondrial activity. The stromal tissues showed little or no mitochondrial oxidative capacity. These findings were backed up using a computer-based informatics approach with gene profiles from over 2,000 breast cancer samples.
In a normal cell, mitochondria give the cell the power it needs to function and divide. However, this study demonstrated that in a cancer cell, mitochondria provide five times as much energy, fueling growth and metastasis of the cancer cells.
Dr. Lisanti said to Cell Cycle:
“Metabolically, the drug Metformin prevents cancer cells from using their mitochondria, induces glycolysis and lactate production, and shifts cancer cells toward the conventional ‘Warburg Effect’. This effectively starves the cancer cells to death.”
Mitochondrial activity could now be used to distinguish cancer cells from normal cells, and establish negative margins during cancer surgery.
Mariel is currently a sophomore at Columbia Grammar and Preparatory School in New York City. She loves learning about science and particularly enjoys genetics, cancer research, radiology, and forensics.