Jason Herschkowitz

  • Jason Herschkowitz


    Dr. Herschkowitz’s research involves integrative approaches, utilizing multidisciplinary techniques including molecular biology, cell biology, mouse models and genomics to elucidate the molecular mechanisms involved in breast cancer progression and therapeutic resistance. Evidence from our laboratory and others has shown that there exist cells within tumors that have an intrinsic resistance to radiation and chemotherapeutics compared to the bulk of the tumor. These cells often referred to as cancer stem cells (CSCs) may also be responsible for metastatic dissemination and tumor dormancy and recurrence. We hypothesize that long noncoding RNAs (lncRNAs) play a critical role in an epithelial-mesenchymal transition (EMT) gene expression program governed in part by RNA-mediated epigenetic regulation leading to resistance to therapies in breast cancer. Our goal, using several model systems, is to first identify and then investigate the mechanisms of action of lncRNAs that regulate the EMT/CSC phenotype of claudin-low breast tumors using siRNA, CRISPR genome engineering, and lentiviral overexpression in vitro and in vivo. We are also employing high resolution RNA fluorescent in situ hybridization, to look at the subcellular localization of these lncRNAs in cultured cells and in clinical embedded breast cancer samples.