Virginia Research Day 2022

Medical Student Research Biomedical

02 The Role Of Perluorooctanoic Acid On Human Liver Cancer Cells

Background: Perfluorooctanoic acid (PFOA) falls under a category of synthetic chemicals known as Per- and polyfluoroalkyl substances (PFAS). These chemicals have a unique chemical structure which grant them both amphipathic and lipophobic properties, as well as increased stability. These unique traits make them ideal for industrial science applications and have been used ubiquitously in this field. However, this stability has led to the accumulation of PFOA in the environment and many organisms, including humans. Effects of PFOA from long-term exposure range from low- birth weight, increased of risk cancer, immune system toxicity, and disruptions in thyroid hormone production. 1 Department of Biochemistry & Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC Osscar Gonzalez Sandoval, BS 1 ; Reshmi Bera, BS 1 ; Kyle DiVito, PhD 1 Corresponding author: ogonzalezsandoval@vt.vcom.edu

Objectives: This study aims to expose HepG2-C3A cells to varying dosages of PFOA during a window of 24-120 hours to determine the effect on viability, apoptosis and expression of cell membrane adhesion protein E-Cadherin. Results: HepG2-C3A cells treated with 5.2µg/ ml of PFOA displayed significant reduction in cellular viability after 120 hours (p<0.03) of exposure. HepG2-C3A cells exposed to low (5.2ng/ml) and high (5.2µg/ml) doses of PFOA displayed no significant increase in apoptotic activity, using the caspase 3/7 mechanism. HepG2-C3A cells were exposed to low (5.2ng/ ml) and high (5.2µg/ml) doses for 120 hours. PFOA displayed no significant decrease E-Cadherin expression at low doses, however,

there was a significant reduction using a high dose (p-value < 0.0003). Conclusion: The data from these experiments indicate higher concentrations of PFOA may influence the viability of cells. The Caspase 3/7 data shows no increase in initiation of apoptosis, even at high concentrations. This may suggest that PFOA causes cell death through other mechanisms or may require longer exposure to see a significant increase in apoptotic activity. The decrease in E-Cadherin expression found in this report may indicate that PFOA has a role in affecting migration of the cell and the susceptibility of tumor invasion.

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