Student Presenter(s): Kaitlin Accardi, Rochelle Ratner, Nushe Hasanramaj, Ariana Nurse, Isaac Sadykov
Faculty Mentor: Niharika Nath
Department: Biological and Medical Sciences
School/College: College of Arts and Sciences, New York City

Cancer causes 10 million deaths worldwide annually according to the WHO. An anticancer candidate Curaxin CBL0137 has been examined against various types of cancers and is in clinical trials. One mechanism by which CBL0137 acts is via a chromatin remodeling complex with the FACT protein. CBL0137 causes FACT to be dispersed from transcribed regions and become trapped in other regions. CBL0137 can also activate p53, which is a tumor suppressor gene that controls the cell cycle by inducing CDK inhibitor p21. It is postulated that CBL0137 can potentially modulate other proteins and pathways for other possible disease treatments. Our objective is to find other transcription factors or P53-associated proteins that are modulated by CBL0137. We examined FACT-based studies in human or mice with CBL0137, identified Gene Expression Omnibus Datasets, performed analyses with untreated and treated datasets and identified a list of differentially expressed genes from a volcano plot. Statistically significant differentially expressed genes were then analyzed for gene ontology and STRING-PPI for potential protein-protein interactions with p53 or selected associated proteins. The proteins FANCB, RFC4, SKP2, AURKA, RRM2B, BUB1, STIL, DHX9, CASC5 are among a few that have the potential to interact with P53 or P53-associated proteins based on combination scores and the strength of observed and expected connections. This may further explain the mechanism of CBL0137 activity.