Kai Brady, a junior biology major at Spelman College, assessed RAC1 dependencies in KRAS-mutant pancreatic cancer cell lines.
Over 90% of pancreatic cancers are driven by activating KRAS mutations that upregulate pathways involved in cell proliferation and migration. Being at the Broad this summer has exposed me to a new community full of collaboration and I have gained a network that will last me a lifetime. The projects I was allowed to take part in are at the forefront of cancer research. My experiences here will forever impact me as a scientist, as I have been opened to a world of innovation and creativity.Despite recent advances in the understanding of KRAS biology, effective therapies for KRAS-driven cancers have not yet been found. Thus, our group is exploring proteins downstream of KRAS as potential proxy targets. We have focused on one of these downstream mediator proteins, RAC1, as an important dependency in KRAS-driven pancreatic cancers. RAC1 is a Rho GTPase that is essential to the reorganization of the actin cytoskeleton in cancer cell proliferation and metastasis. Using pharmacologic and siRNA-based approaches in seven pancreatic cancer cell lines, we investigated the inhibition of RAC1 expression and its ability to decrease pancreatic cancer cell viability. Our goal is to assess RAC1 as a potential therapeutic target for KRAS-driven cancers.
Project: Validating RAC1 dependency in KRAS-driven pancreatic cancer
Mentors: Raymond Ng, Rita Sulahian, Srivatsan Raghavan, Cancer Program