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2016 DEPARTMENT OF MEDICINE RESEARCH DAY Title of Poster: Identification of Targetable EMT Markers in Cancer Stem-like Cells Derived from Therapeutic Resistant Melanoma Presenter: William Crosson Division: Hematology-Oncology ☐ Faculty ☐ Fellow ☐ Resident ☐ Post-doc Research Fellow ☐ Graduate Student ☐ Medical Student ☐Other Principal Investigator/Mentor: Ramin Nazarian Co-Investigators: Elyse Berlinberg Thematic Poster Category: Development, Morphogenesis, Cell Growth and Differentiation, Apoptosis, Stem Cell Biology, Carcinogenesis and Cancer Biology Abstract Melanoma is the deadliest form of skin cancer, expected to claim approximately 10,000 lives in 2016. An activating mutation in BRAF(V600E) occurs in 50-60% of melanomas and 7% of all cancers. Despite an unprecedented initial response, patients treated with a highly effective BRAF inhibitor, vemurafenib (FDA approved 2011), acquire drug resistance within 6-9 months. Vemurafenib-resistant sub-lines, derived from BRAFV600E isogenic parental melanoma cells, have altered cell morphology and upregulated PDGFRβ expression. Epithelial-to-mesenchymal transition (EMT), a hallmark of cancer-stem-like cells (CSC), is a potential mechanism that melanomas employ to evade targeted therapy. Through immunocytochemical, immunoblot, and flow cytometric analysis, we investigated the expression profile of EMT biomarkers within parental and resistant melanoma cell lines to determine whether EMT is associated with acquired drug resistance. Our findings indicate CSCs within melanoma populations may serve as progenitor cells for therapy-resistant melanoma sublines. These results demonstrated differential expression of key transcription factors and cell adhesion molecules, potentially indicating the presence of EMT driven CSCs. Furthermore, migration assays indicated that resistant cell lines were significantly more invasive. Our results implicate notable EMT biomarkers in CSCs that can be used as novel targets for diagnosis and treatment of tumor resistance in melanoma patients.
