Akar, SakineDonmez-Altuntas, HamiyetHamurcu, Zuhal2025-05-102025-05-1020220301-48511573-497810.1007/s11033-022-07536-52-s2.0-85131306447https://doi.org/10.1007/s11033-022-07536-5https://hdl.handle.net/20.500.14720/14236Donmez Altuntas, Hamiyet/0000-0001-6473-5813Background The c-myc oncogene, which causes glutamine dependence in triple negative breast cancers (TNBC), is also the target of one of the signaling pathways affected by beta-Escin. Methods and results We sought to determine how c-myc protein affects glutamine metabolism and the proteins, glutamine transporter alanine-serine-cysteine 2 (ASCT2) and glutaminase (GLS1), in beta-Escin-treated MDA-MB-231 cells using glutamine uptake and western blot analysis. Cell viability, colony formation, migration and apoptosis were also evaluated in MDA-MB-231 cells in response to beta-Escin treatment using MTS, colony forming, wound healing, and Annexin-V assay. We determined that beta-Escin decreased glutamine uptake and reduced c-myc and GLS1 protein expressions and increased the expression of ASCT2. In addition, this inhibition of glutamine metabolism decreased cell proliferation, colony formation and migration, and induced apoptosis. Conclusions In this study, it was suggested that beta-Escin inhibits glutamine metabolism via c-myc in MDA-MB-231 cells, and it is thought that as a result of interrupting the energy supply in these cells via c-myc, it results in a decrease in the carcinogenic properties of the cells. Consequently, beta-Escin may be promising as a therapeutic agent for glutamine-dependent cancers.eninfo:eu-repo/semantics/closedAccessApoptosisAsct2Breast CancerBeta-EscinGlutamineGls1MigrationC-MycMda-Mb-231Article498Q3Q37409741535655054WOS:000805077500005