Karla F. Meza-Sosa, Ph.D.

Research

The Lieberman lab explores the role of noncoding ribonucleic acid (RNA) molecules in the cell's response to DNA damage. When cells are exposed to radiation or other DNA-damaging agents, they activate a protein called p53. This protein keeps cells from multiplying and copying mutated DNA, giving them time to repair the problem. However, if the damage is too severe, p53 triggers cell death—a fail-safe response that keeps the cell from forming a tumor. Indeed, p53 is inactivated in half of all human cancers. But p53 does not act alone. Recent studies from Dr. Lieberman's lab indicate that p53 activates a newly discovered long noncoding RNA, which is needed to trigger cell death in response to severe DNA damage. During my postdoctoral fellowship in the lab, I studied the molecular mechanisms by which this RNA, called SPARCLE, assists p53 in its duties by enhancing Caspase3-mediated cleavage of the genotoxic stress sensor protein PARP1, resulting in a higher rate of apoptosis in cancerous cells. Our work was published in the Molecular Cell Journal in January 2022 (PubMed ID: 35104452). Currently, I’m working on the role of noncoding RNA molecules in brain cancer appearance and progression.