Expression Profiling of Epithelial Transcription Factors in Breast Cancer Cell Lines

Maria A. Voronkova, Joseph B. Addison, Morgan Johnson, James H. Fugett, Anna Alappat, Jordan Means*, Kathleen Summers*, and Alexey V. Ivanov

Department of Biochemistry and WVU Cancer Institute, West Virginia University, Morgantown, WV

Presentation Category: Health Sciences (Poster Presentation #124)

Student’s Major: Immunology and Medical Microbiology

Cancer metastasis is the spread of cancerous cells from primary location to other organs and is a major cause of cancer related deaths. 90% of human cancers are of epithelial origin. The Epithelial-to-Mesenchymal Transition (EMT) has been shown to promote metastasis by enabling epithelial cancer cells to acquire such mesenchymal properties as invasion, migration, and resistance to apoptosis. The study of transcription factors (TFs) can uncover the mechanisms by which EMT processes are activated and controlled. Mesenchymal to Epithelial Transition (MET) TFs help promote gene expression leading to the cellular transition of mesenchymal cells. We have previously identified a set of TFs that are downregulated during EMT and hypothesized that they are responsible for maintaining the epithelial state and suppression of EMT. We profiled their expression in a panel of epithelial (luminal and basal) and mesenchymal breast cancer cell lines using real-time qPCR. We found that OVOL1, OVOL2, GRHL1, GRHL2, GRHL3, ELF3, ELF5, and IRF6 were expressed at high levels in majority of epithelial cell lines and almost invariably not expressed in mesenchymal cell lines. In addition, ESR1, GATA3, and FOXA1 were highly expressed in luminal cell lines, as expected. These data suggest that expression of these 11 TFs is associated with the epithelial phenotype and that they could potentially suppress EMT. We plan to test if these TFs can suppress EMT in functional assay by overexpressing them in mesenchymal breast cancer cells. The identification of EMT suppressors will facilitate future efforts to inhibit EMT and metastasis in breast cancer.

Funding: INBRE

Program/mechanism supporting research/creative efforts: Other, INBRE