For years, scientists have observed that tumor cells from certain breast cancer patients with aggressive forms of the disease contained low levels of mitochondrial DNA. But, until recently, no one was able to explain how this characteristic influenced disease progression. Now, University of Pennsylvania researchers have revealed how a reduction in mitochondrial DNA content leads human breast cancer cells to take on aggressive, metastatic properties. The work, published online on November 4, 2013, in the journal Oncogene, breaks new ground in understanding why some cancers progress and spread faster than others and may offer clinicians a biomarker that would distinguish patients with particularly aggressive forms of disease, helping personalize treatment approaches. The study was led by the Penn School of Veterinary Medicine’s Dr. Manti Guha, a senior research investigator, and Dr. Narayan Avadhani, Harriet Ellison Woodward Professor of Biochemistry in the Department of Animal Biology. Additional Penn Vet collaborators included Drs. Satish Srinivasan, Gordon Ruthel, Anna K. Kashina, and Thomas Van Winkle. They teamed with Dr. Russ P. Carstens of Penn’s Perelman School of Medicine and Drs. Arnulfo Mendoza and Chand Khanna of the National Cancer Institute. Mitochondria, the so-called “powerhouses” of mammalian cells, are also a signaling hub. They are heavily involved in cellular metabolism as well as in apoptosis, the process of programmed cell death by which potentially cancerous cells can be killed before they multiply and spread. In addition, mitochondria contain their own genomes, which code for specific proteins and are expressed in coordination with nuclear DNA to regulate the provision of energy to cells.
Login Or Register To Read Full Story