Science University Research Symposium (SURS)

L-Ascorbic acid Induced Upregulation of Pro-Apoptotic Genes in HCT116 Human Colorectal Cancer Cells With and Without Functional p53

Publication Date

2026

College

College of Sciences & Mathematics

Department

Biology, Department of

Presentation Type

Poster Presentation

Abstract

Apoptotic mechanisms have been consistently studied across certain metastatic cell lines as there could be potential therapeutic implications in the future. L-ascorbic acid has been investigated as a potential apoptosis-inducing agent due to its disturbance of the reactive oxygen species (ROS) concentrations in the nucleus of cancer cells. In B-cell Lymphoma cells, the oxidative status of the cysteine 117 residue on MYC can induce EGR1 upregulation, potentially resulting in apoptosis. Differences in the uptake of ascorbic acid’s metabolite, dehydroascorbate (DHA), via increased GLUT1 expression can deplete intracellular glutathione, thus causing cell damage and death. The KRAS mutation in HCT116 causing the increased expression of GLUT1 is necessary to consider when evaluating potential apoptotic mechanisms. As well, the absence of p53 activity has been shown to be required for MYC-EGR1-driven apoptosis. This study, seeks to determine the potential proapoptotic effect of ascorbic acid on HCT116 human colorectal cancer cells with and without functional p53 by assessing the expression of the proapoptotic genes BIM and NOXA, known to stimulate the intrinsic apoptotic pathway. Cells were exposed to 5 mM ascorbic acid for 1 hour then given an extended, 48-hour recovery.  After treatment and recovery, total RNA was isolated, and expression of MYC, EGR1, NOXA, and BIM were assessed by quantitative real-time reverse transcriptase PCR. These studies will contribute to our understanding of p53-independent, MYC-EGR1apoptosis and the potential of that ascorbic acid may be a chemical stimulator of this pathway in human colorectal cancer cells.

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