Science University Research Symposium (SURS)

Publication Date

Winter 2025

College

College of Sciences & Mathematics

Department

Biology, Department of

SURS Faculty Advisor

Dr. Erick Spears

Presentation Type

Poster Presentation

Abstract

The WNT signaling pathway plays a crucial role in the regulation of cell growth and death in the intestinal epithelium and during colorectal carcinogenesis. In the presence of Wnt, MYC is upregulated, which leads to the proliferation of intestinal epithelial cells. Under certain cellular conditions, namely the loss of p53 function common to colorectal tumors, MYC upregulates the expression of the tumor suppressor EGR1, leading to apoptosis. This MYC-EGR1 pathway has been observed in p53-knockout mouse embryonic fibroblasts but has yet to be observed in human cells. These studies aim to assess the activity of the MYC-EGR1 pathway in human variants of the HCT116 human colorectal cancer cell line with and without functional p53 (p53+/+ and p53-/-, respectively). We transduced these sister cells line with shRNA targeting MYC or EGR1 expression or with a control, nontargeting shRNA. Transduction was verified with a GFP transduction marker. After transduction, RNA was isolated and expression of TP53 (the p53 gene), MYC and EGR1 were assessed by quantitative real-time RT-PCR analysis to assess the activity of the MYC-EGR1 pathway in these HCT116 variant cell lines. We validated the absence of TP53 gene expression in the p53-/- cells indicating these cells as a good model for assessment to the MYC-EGR1 pathway in human cells. We further assessed whether the knockdown of MYC in each of the subject cell lines impacted the expression of EGR1. The identification of the MYC-EGR1 pathway in human colorectal cancer cells would represent the first step toward potentially identifying a novel therapeutic target for colorectal cancer.

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