Under stressful conditions, presence of high levels of HER2 protein causes a decrease in autophagy

Apr 6 2011

Research from The Cancer Institute of New Jersey (CINJ) on biological pathways that govern progression and treatment responsiveness of HER2 positive breast cancer is being presented at the 102nd Annual Meeting of the American Association for Cancer Research (AACR) being held in Orlando this week. CINJ is a Center of Excellence of UMDNJ-Robert Wood Johnson Medical School.

The focus of this poster presentation is the protein known as Human Epidermal growth factor Receptor 2 (HER2/neu) and the role it plays in breast cancer aggressiveness, poor clinical outcome and chemotherapy resistance. About thirty percent of breast cancers have high levels of the HER2 protein.

This current research by lead investigator Fred Lozy, a member of the Dr. Vassiliki Karantza laboratory at CINJ, finds that under stressful conditions, the presence of too much HER2 causes a decrease in autophagy. Autophagy is an energy recycling process that helps cells to survive, but under certain conditions can also go awry and result in tumor formation. Normally, a decrease in this process would hinder a cell's ability to survive; however, in this case, utilizing laboratory models and gene expression profiling, Lozy and colleagues found that these cells alter other cellular processes to compensate for the lack of autophagy. Consequently, changes in these cellular processes may increase breast cancer growth, metastasis, and/or enable the disease to become resistant to chemotherapy.

"Identifying altered pathways is an important step that may help scientists discover how breast cancer progresses as well as find new targets for breast cancer therapies," noted Lozy, who is also a PhD graduate student in the joint Graduate Program in Cell and Developmental Biology at the UMDNJ-Graduate School of Biomedical Sciences at Robert Wood Johnson Medical School and Rutgers, The State University of New Jersey.