Myc Protein Expression in Response to Docosahexaenoic Acid

Abstract

Breast cancer is a commonly diagnosed cancer and targets 1 in 8 women in the United States, annually. Certain changes in DNA can induce normal cells to become abnormal, and a contributor to this is a gene called Myc, which has shown to be overexpressed in many cancers, including breast cancer. Myc was one of the first discovered oncogenes and it functions as a transcription factor that regulates nearly 15% of the genome. When Myc is mutated in cancer, called c-Myc, it functions abnormally and activates pro-survival and pro-proliferative pathways. Although decades of research have proven that it could serve as a promising chemotherapeutic target because it plays such an important role in cellular division, metabolism, and apoptosis, there has been no therapeutic success. Its dysregulation causes uncontrolled cell growth, which is a hallmark of cancer. Furthermore, overexpression of GLUT glucose transporter proteins can facilitate the development of many cancer types due to higher than normal glucose metabolism, named the Warburg effect. Nutritional supplementations, such as omega-3 (n-3) polyunsaturated fatty acids (PUFAs), have been known to lower the chances of developing cancer, especially in breast cancer. Preliminary evidence suggests that docosahexaenoic acid (DHA), an omega-3 fatty acid, has been found to inhibit cancer cell growth and alters the phosphorylation status of Myc. Analysis of Myc phosphorylation sites, which is critical for determining downstream Myc targets will provide a better understanding of the anti-cancer properties of DHA and examine the consequences of these alterations in breast cancer. Contributions to this research that has vast benefits can improve the quality of life for breast cancer victims.