儿童癌症在低收入国家的治愈率可能仅有15％，说明需要更便宜的治疗选项。氟西汀是一种经过充分安全测试的药物，可能靶向sigma-1受体（σ1-R）。使用人类白血病细胞系Jurkat，我们使用XTT和尝试蓝染色研究了氟西汀对细胞存活的影响。使用AnnexinV / PI染色和西方印迹分析caspase分裂来测量细胞凋亡。测量Jurkat细胞在响应PHA / PMA时的IL-2分泌使用ELISA，并使用Western印迹法测定AKT / pAKT和σ1-R的表达。氟西汀诱导细胞凋亡和G-2细胞周期停滞。氟西汀剂量依赖性降低IL-2分泌，并可通过σ1-R拮抗剂BD1047进一步增强（P <0.05）。氟西汀在治疗后6小时抑制pAKT（P <0.05）。 Jurkat细胞中σ1-R的表达在12至48小时之间显示明显增加（P <0.05）。与此同时，自噬显著增加。氟西汀可能具有治疗急性白血病的潜力。与σ1-R拮抗剂联合治疗可增强氟西汀诱导的细胞凋亡，可能通过靶向AKT磷酸化和自噬激活来实现。

Childhood cancer has a cure rate of as low as 15% in low-income countries, suggesting a need for cheaper treatment options. Fluoxetine is a thoroughly safety-tested drug that may target the sigma-1 receptor (σ1-R).Using the human leukemic cell line, Jurkat, we investigated the effects of fluoxetine on cell survival using XTT and trypan blue staining. Apoptosis was measured using AnnexinV/PI staining and western blot analysis of caspase cleavage. IL-2 secretion of Jurkat cells in response to PHA/PMA was measured using ELISA, and the expression of AKT/pAKT and the σ1-R were measured using western blotting.Fluoxetine-induced apoptosis and G-2 cell cycle arrest. Fluoxetine reduced IL-2 secretion dose-dependently and could be further potentiated by σ1-R antagonist BD1047 (P < 0.05). Fluoxetine inhibited pAKT six hours post-treatment (P < 0.05). The expression of the σ1-R showed a significant increase between 12 to 48 hours in Jurkat cells (P < 0.05). At the same time, there was a substantial increase in autophagy.Fluoxetine may have the potential for acute leukemia treatment. Co-treatment with a σ1-R antagonist increases fluoxetine-induced apoptosis, possibly targeting AKT phosphorylation and autophagy activation.