Steven M. Frisch
West Virginia University Health Science Center
United States of America
Works as Professor in Biochemistry.
Our lab has contributed to an understanding of cancer biology in two areas. The first involves transcription factors that promote or suppress the oncogenic Epithelial-Mesenchymal Transition (EMT). EMT is a gene expression program that confers tumor cell invasion, metastasis, drug-resistance and cancer stemness. Currently, we are focusing on a newly discovered factor that ubiquitously reverses EMT. The second area stems from our discovery that normal epithelial cells –but not tumor cells that have undergone EMT – die via apoptosis when detached from their extracellular matrix. This process, called “anoikis”, safeguards against tumor metastasis. We are currently investigating intracellular metabolic changes accompanying EMT that impact upon anoikis. A recent, major focus area in the Frisch lab is the control of epigenetic marks, especially histone modifications, during EMT, and how these impact upon drug resistance and tumor recurrence. Our projects are highly translational, with discoveries informing the development of novel drugs to suppress metastasis and tumor recurrence in patients.
Cieply B, Koontz C, Frisch SM. "CD44S-hyaluronan interactions protect cells resulting from EMT against anoikis". Matrix Biol. 2015 Oct;48:55-65. doi: 10.1016/j.matbio.2015.04.010. Epub 2015 Apr 30.PMID:25937513
Farris, J, Pifer, P, Zheng, L, Gottlieb,E, Denvir,J and Frisch, SM. "GRHL2 reverses metabolic changes induced by the oncogenic epithelial-mesenchymal transition: effects on anoikis". Mol Cancer Res. 2016 Apr 15. pii: molcanres.0050.2016. [Epub ahead of print]
Pifer PM, Farris JC, Thomas AL, Stoilov P, Denvir J, Smith DM, Frisch SM. "Grainyhead-like-2 inhibits the coactivator p300, suppressing tubulogenesis and the epithelial-mesenchymal transition". Mol Biol Cell. 2016 Jun 1. pii: mbc.E16-04-0249. [Epub ahead of print]