Publication Date

Spring 4-22-2026

Presentation Length

Poster/Gallery presentation

College

College of Sciences & Mathematics

Department

Biology, Department of

Student Level

Undergraduate

Faculty Mentor

Erick Spears

Presentation Type

Poster

Summary

Colorectal cancer progression is influenced by dysregulated signaling pathways that affect cell proliferation and migration. One important pathway is WNT signaling, which promotes MYC expression and contributes to tumorigenesis. In the absence of functional p53, MYC has been shown to induce the tumor suppressor gene EGR1, leading to EGR1-driven apoptosis rather than proliferation. This noncanonical activity of MYC has been termed the MYC-EGR1 pathway and has only been observed in the absence of functional p53, a well-known genetic aberration associated with colorectal cancer progression. Of particular interest is the impact of the expression of EGR1 on colorectal cancer cell malignancy as determined by invasive migration. We used variant HCT116 colorectal cancer cells with either wild-type p53 (p53+/+) or a knockout at the TP53 locus (p53−/−) to assess whether EGR1 can impact invasive migration of these cells. To assess the role of EGR1 in cell migration, shRNA knockdown of EGR1 expression was used and migration was assessed using a standard cell culture wound-healing assay, a scratch assay. Both p53+/+ and p53−/− cells exhibited progressive wound closure, indicating that migration occur regardless of p53 status. Further analysis will assess the role EGR1 in this migration using the targeted shRNA. These studies will help in the understanding of the role that EGR1 plays in invasive colorectal cancer cell migration. Further study is required to establish the functioning of the MYC-EGR1 pathway in these cells but understanding the role of EGR1 in cell migration will offer some insight into the mechanisms involved in invasive migration of colorectal cancer cells. These studies contribute to a battery of studies that aim to understand the role of the MYC-EGR1 pathway in human colorectal cancer cells and the association of this pathway with colorectal malignancy.

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