Mechanistically, treatment downregulated key nucleotide biosynthesis genes (<i>DHFR</i>, <i>TK1</i>) and the glycolytic enzyme gene (<i>ENO1</i>), while upregulating the oxidative stress response gene <i>SLC7A11</i> (18.32-fold), suggesting disruption of cancer metabolic pathways. This evidence concerns the gene ENO1 and cancer.