Science University Research Symposium (SURS)
Publication Date
11-2025
College
College of Sciences & Mathematics
Department
Biology, Department of
SURS Faculty Advisor
Erick Spears
Presentation Type
Poster Presentation
Abstract
Colorectal cancer progression is driven in part by dysregulated signaling pathways that alter cell growth and migration. One key pathway is the Wnt signaling pathway, a key regulator in colorectal tumorigenesis, which promotes MYC overexpression, leading to uncontrolled proliferation. Interestingly, in the absence of p53, MYC has been found to induce expression of the tumor suppressor gene EGR1, shifting the cellular response toward apoptosis rather than growth. This study investigates the MYC–EGR1 pathway in HCT116 colorectal cancer cells with either wild-type (p53+/+) or knockout of the TP53 gene (p53−/−). Early findings indicate that p53+/+ cells exhibit faster initial growth compared to p53−/− cells; however, p53−/− cells gradually increase their growth rate over successive passages. To assess whether the cells were migrating or proliferating, we performed wound-healing assays using HCT116 colorectal cancer cells with both wild-type (p53+/+) and knockout (p53−/−) and captured images at 0-, 24-, and 48-hours post-wound. Both p53+/+ and p53−/− cells exhibited progressive closure of the scratch, indicating the occurrence of migration regardless of the p53 status. To further examine the functional contributions of MYC and EGR1, we used Lentiviral shRNA to knock down MYC and EGR1. We examined the effects of these genes on cell proliferation and migration through wound-healing assays and imaging. These observations suggest that HCT116 cells migrate in the presence and absence of p53. Further analysis of the MYC-EGR1 pathway in these cellular contexts is still ongoing.
Recommended Citation
Faragalla, Mehrael; Barsoum, Karen; and Spears, Erick, "Characterization of Colorectal Cancer Cell Responses Using a Wound-Healing Scratch Assay Model on Wild-type (p53 +/+) and Knockout (p53 -/-)" (2025). Science University Research Symposium (SURS). 257.
https://repository.belmont.edu/surs/257
