Chemotherapy is a key part of the standard treatment regimen for triple-negative breast cancer patients whose cancer lacks expression of estrogen and progesterone receptors and the human epidermal growth factor receptor 2 (HER2). While many patients respond well to chemotherapy, a significant fraction of those treated are resistant to chemotherapy or will develop recurrent tumors that are chemoresistant. In this issue of JCI Insight, a research team led by Mercedes Rincon at the University of Vermont identified low expression of methylation-controlled J protein (MCJ) as a marker of poor response to chemotherapy. In a prospective study of 62 breast cancer patients, they demonstrated that MCJ expression correlates with pathological and clinical responses to neoadjuvant chemotherapy. Further, by analyzing a large clinical data set from breast cancer repositories, they found that breast cancer patients with low-MCJ-expressing tumors had reduced relapse-free survival. Lastly, they examined a mammary tumor mouse model and showed that mice deficient in MCJ had larger tumors and increased chemoresistance. Their study suggests that MCJ may be useful as a marker of chemotherapy response and could be a potential therapeutic target for breast cancer treatment.
Deficiency of mitochondrial modulator MCJ promotes chemoresistance in breast cancer
University of Vermont
View this article at: http://insight.
JCI Insight is the newest publication from the American Society of Clinical Investigation, a nonprofit honor organization of physician-scientists. JCI Insight is dedicated to publishing a range of translational biomedical research with an emphasis on rigorous experimental methods and data reporting. All articles published in JCI Insight are freely available at the time of publication. For more information about JCI Insight and all of the latest articles go to http://www.