Understanding the role of MYC in invasive migration of p53-variant human colorectal cancer cells

Publication Date

Spring 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 (CRC) is the second leading cause of cancer-related death in the U.S. Disease progression is driven in part by dysregulated intracellular signaling pathways that alter cell proliferation and migration. The key pathway in CRC initiation and progression is the Wnt signaling pathway, which promotes MYC expression, leading to uncontrolled proliferation and invasive cell migration. Interestingly, in the absence of the cell cycle checkpoint regulator p53, MYC has been found to induce expression of the tumor suppressor gene EGR1, shifting the cellular response toward apoptosis rather than proliferation. This pathway is of particular interest in CRC as the progressive mutations associated with tumor development often include the loss of functional p53 from colorectal tumor cells. That said, the functional consequence of this MYC-EGR1 pathway in human colorectal malignancy remains incompletely understood. Specifically, the role of MYC in the invasive migration of tumor cells and the potential activation of the MYC-EGR1 pathway in tumor cells lacking functional p53 has not been observed. This study investigates the role of MYC in migration of HCT116 colorectal cancer cells with either wild-type (p53+/+) or knockout of the TP53 gene (p53−/−). Preliminary studies indicate that knockdown of MYC in parental HCT116 cell lines does not impact the migration of these cells. To investigate the functional contributions of MYC to migration of these cells, we employed lentiviral shRNA to knock down MYC and examined the effects on cell migration via a standard cell culture wound healing assay.  Further analysis will compare the migration of these cells lacking functional p53 and assess the activity of the MYC-EGR1 pathway in these cellular contexts. Understanding the activity of the MYC-EGR1 pathway in human CRC cells may offer some insight into mechanisms driving colorectal malignancy and the potential for novel therapeutic approaches.

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