Science University Research Symposium (SURS)

Publication Date

Summer 11-10-2024

College

Sciences and Mathematics, College of

Department

Biology, Department of

SURS Faculty Advisor

Dr. Erick Spears

Presentation Type

Poster Presentation

Abstract

Cancer is often initiated by genetic alterations that affect cellular proliferation, survival, and differentiation. Colorectal cancers are specifically initiated and driven by mutations affecting the Wnt signaling pathway and mutations in the CTNNB1 gene are the second most common of these mutations found in colorectal cancers. Among these, mutations in the CTNNB1 gene, encoding β-catenin, frequently lead to dysregulated Wnt signaling, a hallmark of colorectal cancer. The proto-oncogene MYC and the early growth response gene EGR1 are known to be critical downstream effectors of several oncogenic pathways. MYC is a known β-catenin target gene and under certain cellular contexts, EGR1 is a target of MYC. However, the interaction between MYC, EGR1, and mutated CTNNB1 in the context of wild-type p53, a crucial tumor suppressor, remains poorly understood. In this study, we investigate the expression patterns of MYC and EGR1 in colorectal cancer cells harboring an oncogenic mutation in CTNNB1 with normal p53 function. Using quantitative real-time RT-PCR, we examined the expression of MYC and EGR1 in colorectal cell lines with and without an oncogenic mutation in CTNNB1 but with normal p53 function. Our findings demonstrate that the oncogenic CTNNB1 mutation significantly upregulates MYC expression, consistent with its role in promoting cell growth. In contrast, EGR1 expression showed a complex regulation. These results highlight the complex interaction between MYC, EGR1, CTNNB1, and p53 in colorectal cancer that requires further study to understand the role of the MYC-EGR1 pathway in Wnt-driven colorectal cancers. The hope is to offer therapeutic insights that might target this pathway in patients with specific genetic backgrounds.

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