DeJuana Ford
Hi, my name is DeJuana Ford. I grew up in Newnan, Georgia and went to college at the University of Georgia in Athens, where I graduated with a degree in Genetics.
I have been passionate about science for as long as I can remember, but I became interested in the field of human genetics in particular after my 9th grade biology teacher gave a lecture on how scientists use genetic markers to track human migration patterns.
For over ten years, my mother has battled systemic Scleroderma, which is an autoimmune disorder. I’ve been actively involved in an organization that provides support to Scleroderma patients. Watching my mother and other patients struggle to overcome the daily obstacles associated with incurable chronic illness inspired me to use my passion for science to explore questions that might improve people’s lives. Working in Dr. Melissa Davis’ lab as an undergraduate further cultivated my passion for the process of research and led me to seek a career in academic research.I am most interested in the field of human genetics, especially as it relates to the study of autoimmune disease, immunology, and cancer immunology.
Ultimately, I aim to have a career that incorporates academic research, teaching, and community outreach. As a researcher, my goal is to gain a better understanding of the genetic and environmental factors which drive the development of autoimmune diseases.
I joined the PREP program, because I was seeking opportunities to gain additional laboratory and research experience and to further enhance my communication skills. These experiences will prepare me to maximize my graduate education and ultimately to be a highly effective independent researcher.
PREP@UGA’s focus on infectious diseases has been especially beneficial for me, as I have a variety of opportunities to explore my interest in immunology.
I look forward to gaining excellent mentorship, learning new laboratory techniques, and building upon my scientific knowledge over the course of this year as a PREP@UGA scholar.
My faculty mentor is Dr. Melissa Davis in the Department of Genetics.
For the past decade, Dr. Davis has worked to gain a better understanding of the molecular and environmental factors driving tumor aggressiveness and breast cancer survival disparities. My project is focused on understanding the role that insulin-like growth factor pathway genes play in triple-negative breast cancer, which is a breast cancer subtype characterized by aggressive tumors that are unresponsive to hormone-based targeted therapies. Insulin-like growth factors, or IGFs are structurally similar to insulin, but are distinct in that they associate with a set of binding proteins that regulate their activity.
Recent studies have linked breast tumor aggressiveness with increased levels of IGF-II protein expression. Prior to becoming a PREP scholar, I along with other members of the Davis lab, observed that IGFBP6, IGF-II’s preferred binding partner demonstrates distinct patterns of expression and subcellular localization in triple negative breast cells.
Specifically, we noticed that in triple-negative cells, IGFBP6 tends to form aggregates at the edge of the nucleus and co-localize with IGF-II. This is significant, because exclusion of these aggregates from the nucleus could limit IGFBP6’s IGF-II-independent, pro-apoptotic activities within the nucleus. Also, IGF-II’s association with IGFBP6 might be prolonging the half-life of IGF-II, thus promoting cancer cell growth.
To further investigate this pattern, I used RNA interference to reduce IGFBP6 mRNA expression in cells derived from triple-negative tumors. To accomplish this, I extracted RNA from triple-negative breast cells and used cDNA synthesis, PCR, and finally, a transcription reaction to synthesize a double-stranded RNA fragment specific to IGFBP6. After transfecting triple-negative cells with the double-stranded RNA, I observed IGF-II expression and subcellular localization in these cells.
I hypothesized that IGF-II would be more evenly distributed throughout the cytoplasm after the IGFBP6 knockdown, and my preliminary data seem to support this hypothesis. This is significant, because it suggests that distinct IGFBP6 expression patterns have the potential to impact IGF-IIs cancer cell growth-promoting activities.
My next set of experiments will use qPCR to access whether the IGFBP6 knockdown in these cells impacted the expression of two anti-apoptotic, downstream targets of IGF-II. Taken together, these data will give us a better understanding of the molecular mechanisms by which the insulin-like growth factor pathway might impact triple-negative breast cancer.
My name is DeJuana Ford, and I am a PREP@UGA scholar.