Science University Research Symposium (SURS)

MYC-EGR1 Pathway in Growth of HCT116 cells With and Without Functional p53

Publication Date



Sciences and Mathematics, College of


Biology, Department of

SURS Faculty Advisor

Erick Spears

Presentation Type

Poster Presentation


Colorectal cancer is the second most common cause of cancer death across the population. Most colorectal cancers are initiated by mutations in the Wnt-signaling pathway. MYC is a target gene of the Wnt-signaling pathway and a well-described oncogene that is often upregulated in colorectal and other malignancies. Under certain cellular contexts, specifically in the absence of functional p53, MYC is known to stimulate the expression of EGR1 resulting in apoptosis. While the MYC-EGR1 pathway has been studied in rodent cells in a synthetic knockout system, we were interested in understanding the effect of this pathway on human colorectal cancer cells. To assess the role of the MYC-EGR1pathway on the growth of human colorectal cancer cells, we employed HCT116 sister cell lines with and without the functional TP53 gene. The expression of either MYC or EGR1 was specifically and temporarily knocked down using targeting siRNAs for each of the pathway components. Serum starved HCT116 p53+/+ and p53-/- cells were transduced with siRNAs targeting MYC or EGR1 expression and proliferation was assessed. These studies are furthering our understanding of an understudied MYC-EGR1 pathway and its role in colorectal cancer cell cycle.

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