Daniel L. Kiss, PhD

The research interests of my lab lie in the changes that occur in the RNA and molecular biology of cells when cellular stress responses converge to cause or exacerbate cardiovascular disease or cancer. I am building a two-pronged collaborative group that leverages RNA molecular biology tools with both specialized and traditional RNA sequencing approaches combined with long-read sequencing to elucidate how these RNA-mediated changes occur. For cytoplasmic RNA recapping, my work aims to determine the regulators that determine the conditions under which, and position(s) where, an RNA is recapped in the cytoplasm. My lab uses both transcriptome-wide (microarrays, RNA-seq and ribosome profiling) and targeted methods (qPCR, polysome gradients, etc.) to understand how cytoplasmic capping drives oncogenic transformation and stress responses linked to cardiovascular diesease. Ultimately, I aim to uncover the evolutionary role of cytoplasmic RNA recapping, to decipher the selection, generation, and regulation of recapping sites, and to develop cytoplasmic recapping-based drug responsiveness screens and/or RNA therapeutics. The other part of my lab focuses on how the FHIT tumor suppressor modulates the translation of the transcriptome in cancer. My work has shown that expression of the FHIT protein results in translational changes for several known cancer-linked mRNAs. Further, that translational regulation is often driven by the 5’ translation leader sequence of the mRNA. For my future FHIT research, I plan to build upon my recently published works by expanding ribosome profiling into FHIT negative patient tumor samples and by developing better cell lines where FHIT expression is more tightly regulated.