The Effect of (−)‐Epigallocatechin‐3‐gallate (EGCG) on Cell Viability and Protein Expression in Human Pancreatic Cancer Cells (Panc‐1) and Rat Osteosarcoma Cell Cultures (UMR 106‐01 BSP)

Abstract

Traditional treatment of cancer includes surgery, radiation, and chemotherapy. There are many studies regarding how cancer cells respond to various treatments. However, not many studies have been done on how cancer cells respond to natural compounds such as (−)‐Epigallocatechin‐3‐gallate (EGCG), a potent ingredient of green tea. In this study, it was hypothesized that EGCG inhibits cell viability of both human pancreatic (Panc‐1) and rat osteosarcoma, UMR 106‐01 BSP (UMR) cell cultures, inhibits the expression of Panc‐1 CXCR‐4 and VEGF‐A proteins in Panc‐1 cell cultures, and the expression of the oncoproteins MYC and PD‐L1 in UMR cell cultures. Briefly, Panc‐1 and UMR cell cultures were routinely passaged, treated with different concentrations of EGCG (0, 20, 40, 60, 80 and 100 μM) in 6 well plates, then incubated for 48 hours at 37 degrees Celsius under humidification and 5% carbon dioxide infusion. At the end of the experiment, all cells were counted using the LUNA Automated Cell Counter (Logos Biosystems). Upon electrophoresis of experimental samples, Western blotting technique was employed to identify the expression of the Panc‐1 proteins (CXCR‐4, VEGFA) and the UMR oncoproteins (MYC and PD‐L1). F test ANOVA was used to compare variances and all values in the results were expressed as means ±SD. Cell viability results from the Panc‐1 and UMR cell lines showed a decrease at the higher concentrations (80 and 100 μM EGCG). The results of the Western blotting technique showed that the expression of Panc‐1 proteins and UMR oncoproteins were inhibited when treated with EGCG. The cell viability results suggest that EGCG may provide a therapeutic effect on both cancer cells lines at higher concentrations. Results of the Western blotting suggest that EGCG may exert its inhibitory effects on Panc‐1 and UMR cell viability through the regulation of Panc‐1 proteins and UMR oncoproteins.Support or Funding InformationThis work was made possible by support from the Ryckman Endowment Student Research Fund of the Biology Department of La Sierra University.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.