Ongoing Project
Histone Demethylases in Cancer Cell Plasticity
Ongoing Project
Histone Demethylases in Cancer Cell Plasticity
Cancer stem cells are intrinsically resistant to most therapies. Through a collaboration with leading synthetic chemists, we are investigating and developing compounds that selectively eliminate cancer stem cells through non-apoptotic mechanisms.
Collaborators
Dr. Michael Lewis, Baylor College of Medicine
Josh Newby, Patient Advocate
Regulators of Histone Methylation Facilitate EMT Reversal
Histones are proteins which facilitate the condensation of DNA in the nucleus. Tight regulation of the accessibility of the DNA is essential for appropriate gene expression. One mechanism underlying this is the post-translational modification of histones, termed the histone code. We have demonstrated that EMT drives genome-wide changes in the histone methylation landscape and that these changes underlie the changes in expression of thousands of genes (Malouf and Taube et al. 2013) and that a histone demethylase is responsible for remodeling bivalency across the genome in cancer stem cells (Taube and Sphyris et al. 2017). We are working to characterize the specific roles of proteins which ‘write’ the histone code, proteins which ‘read’ the histone code, and proteins that ‘erase’ the histone code in epithelial-mesenchymal plasticity.
Funded by Susan G. Komen #CCR18548469