MYC and EGR1 Expression and Proliferation of Colorectal Cancer Cell Lines
Sciences and Mathematics, College of
Biology, Department of
SURS Faculty Advisor
The American Cancer Society estimates that in 2023, one person every five minutes will be diagnosed with colorectal cancer. An abundance of research has been conducted on the relationship between the Wnt/β-Catenin Signaling Pathway and colorectal cancer. In this pathway, the growth-stimulating protein Wnt binds to a receptor called Frizzled, which transduces a signal. This ultimately results in β-Catenin-driven expression of genes associated with cell proliferation. One such gene is MYC, which is said to be the most important proliferative target gene of the Wnt pathway in colon cancer. While MYC expression is typically associated with cell cycle progression, under certain cellular contexts it has been shown to stimulate apoptosis by stimulating the expression of the tumor suppressor EGR1. Previous literature has suggested that EGR1 is a direct transcriptional target of MYC but does not contain the canonical MYC binding element in its promoter, and its expression is only activated in the absence of other cell cycle control elements. In this project, we seek to determine whether the MYC-EGR1 pathway is active in HCT116 colorectal cancer cell lines with wildtype and mutant CTNNB1 (the β-catenin gene). Using RNA interference, we decreased the expression of MYC or EGR1 and observed proliferation in these cell lines. We also evaluated the expression of MYC and EGR1 in these cells during the proliferation assays to determine if changes in β-catenin activation are impacting these downstream effectors. With these studies, we hope to understand whether the cellular context associated with colorectal cancer activates this unique MYC-EGR1 pathway and whether it changes proliferation in these cells.
Angel, Akanee; Wallace, Libby; and Spears, Erick, "MYC and EGR1 Expression and Proliferation of Colorectal Cancer Cell Lines" (2023). Science University Research Symposium (SURS). 86.