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• W4283749757 startingPage "115159" @default.
• W4283749757 abstract "Conventional and targeted cancer therapies may induce a cellular senescence program termed therapy-induced senescence. However, unlike normal cells, cancer cells are able to evade the senescence cell cycle arrest and to resume proliferation, driving tumor recurrence after treatments. Cells that escape from therapy-induced senescence are characterized by a plastic, cancer stem cell-like phenotype, and recent studies are beginning to define their unique metabolic features, such as glutamine dependence. Here, we show that the antineoplastic drug trabectedin suppresses escape from therapy-induced senescence in all cell lines studied, and reduces breast cancer stem-like cells, at concentrations that do not affect the viability of senescent tumor cells. We demonstrate that trabectedin downregulates both the glutamine transporter SLC1A5 and glutamine synthetase, thereby interfering with glutamine metabolism. On the whole, our results indicate that trabectedin targets a glutamine-dependent cancer stem-like cell population involved in evasion from therapy-induced senescence and suggest a therapeutic potential for trabectedin combined with pro-senescence chemotherapy in tumor treatment." @default.
• W4283749757 created "2022-07-02" @default.
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• W4283749757 date "2022-08-01" @default.
• W4283749757 modified "2023-10-17" @default.
• W4283749757 title "Trabectedin suppresses escape from therapy-induced senescence in tumor cells by interfering with glutamine metabolism" @default.
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• W4283749757 doi "https://doi.org/10.1016/j.bcp.2022.115159" @default.
• W4283749757 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35780827" @default.
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