Science University Research Symposium (SURS)
Publication Date
Fall 11-9-2026
College
College of Sciences & Mathematics
Department
Biology, Department of
SURS Faculty Advisor
Dr. Erick Spears
Presentation Type
Poster Presentation
Abstract
The tumor suppressor p53 primarily regulates cell growth and promotes cell death in the event of excessive cell damage. Through the Wnt signaling pathway, expression of the proto-oncogene MYC drives normal cell proliferation in the colorectal epithelium. In colorectal tumors, dysregulation of MYC results in inappropriate proliferation and accumulation of mutations including inactivation of the TP53 gene, thus resulting in a loss of p53 function. Interestingly, dysregulation of MYC has also been shown to induce apoptosis through upregulation of EGR1 expression in the absence of functional p53. The mechanism of EGR1-stimualted apoptosis under these conditions is still a subject of study. Studies have shown EGR1 regulating expression of NOXA and BIM, two pro-apoptotic proteins of the BCL-2 protein family known to stimulate the intrinsic apoptotic pathway. In these studies, quantitative real-time reverse transcriptase PCR (qRT-PCR) is used to assess the expression of TP53, MYC, EGR1, NOXA, and BIM in HCT116 human colorectal cancer cells with and without functional, providing insight on the relationship between the expression of these genes in the presence and absence of p53. . Understanding the molecular switch that changes MYC from an oncogenic driver to a proapoptotic factor could lead to targeted therapies for colorectal cancers in the future.
Recommended Citation
Boshra, Youssef S.; Mousley, Sojda; and Spears, Erick A. PhD, "Investigating the Role of p53 in MYC-EGR1-Mediated Regulation of NOXA- and BIM-Associated Apoptotic Pathways in HCT116 Cells." (2026). Science University Research Symposium (SURS). 358.
https://repository.belmont.edu/surs/358
