The Role of hnRNPM in EMT and Breast Cancer Metastasis

Friday, February 17, 2017
Exhibit Hall (Hynes Convention Center)
Sabrina Gjerswold-Selleck, Bergen County Academies, Hackensack, NJ
Tumor metastasis is currently the leading cause of cancer-related deaths. A developmental process that initiates the metastatic state is the epithelial-mesenchymal transition (EMT) whose initiation and progression are not well understood. Understanding EMT requires studying the roles of proteins involved, such as hnRNPM (heteronuclear ribonucleoprotein M), a protein involved in alternative splicing in tumor cells. This study addresses the role of hnRNPM through its downregulation in breast cancer cells in TGFβ induced EMT. The protein hnRNPM was stably downregulated in a triple negative breast cancer cell line, MDA-MB-231, through a transfection with hnRNPM shRNA plasmid. The progression of EMT was analyzed through ELISA assays monitoring the expression of proteins indicative of mesenchymal-specific cells, specifically, for example, the protein vimentin. A migration assay showed that downregulation of hnRNPM decreased migration of breast cancer cells. Further, cell viability was analyzed and data showed that cells proliferated most significantly when hnRNPM was knocked down and without TGFβ treatment, and the least when control cells were treated with TGFβ. These findings demonstrate a novel molecular mechanism through which tumor metastasis is potentiated by hnRNPM expression, and role that this protein can potentially have in tumor growth. Research of this nature will have applications in the treatment of triple negative breast cancer.