β-Escin Reduces Cancer Progression in TNBC by Inhibiting Glutamine Metabolism Through Downregulation of c-myc.

Abstract The oncogene c-myc, which causes glutamine dependence in TNBC, is also the target of one of the β-Escin affected signaling pathways. We sought to determine how c-myc protein affects glutamine metabolism and proteins ASCT2 and GLS1 in β-Escin-treated MDA-MB-231 cells by glutamine uptake and western blot analysis. We also evaluated cell viability, colony formation, migration and apoptosis in MDA-MB-231 cells in response to β-Escin treatment using MTS, colonoy forming, wound healing, and Annexin-V assay. We determined that β-Escin decreased glutamine uptake and decreased myc and GLS1 protein expressions, conversially increased the expression of ASCT2. In addition, we determined that this inhibition of glutamine metabolism decreases cell proliferation, colony formation and migration, and induces apoptosis. In this study, it has been revealed that β-Escin inhibits glutamine metabolism through c-myc in MDA-MB-231 cells, by causing a reduce in the carcinogenic properties of the cells as a result of interrupting the energy source of these cells. As a result, β-Escin can be used as a therapeutic agent in glutamine dependent cancers.