Identification of Ferroptosis Induction by Treating Atorvastatin in B16F10.OVA Cells

Min Seok Kim, In Ho Im, Yun Hwa Jeong, Seung Hyun Kim, Young-Chang Cho, Jeong Uk Choi
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Abstract

In this study, we identified whether atorvastatin could induce ferroptosis or not in B16F10.OVA cells, which is being used to treat hypercholesterolemia. To demonstrate this, we treated the mouse melanoma cell line B16F10.OVA with atorvastatin at varying concentrations, spanning from low to high, followed by a 24-hour culture period. In the group treated with atorvastatin in our experiment, we observed a decrease in cell viability that was dependent on the concentration of the treatment, when compared to the control group. The IC50 value of atorvastatin in B16F10.OVA cells was determined to be 49.89 μM. Compared to the control group, treatment with atorvastatin resulted in a concentrationdependent increase in the generation of reactive oxygen species and the accumulation of iron ions. Moreover, atorvastatin treatment exhibited a concentration-dependent increase in the population of apoptotic cells and the expression of calreticulin, significantly surpassing that of the control group. The analysis of ferroptosis-related protein expression levels revealed a notable decrease in the expression of GPX4 in the group treated with atorvastatin, as compared to the control group. These findings strongly suggest that atorvastatin holds promise as a potent anti-cancer agent capable of inducing ferroptosis in melanoma cells.
阿托伐他汀治疗B16F10诱导铁下垂的鉴定。卵子细胞
在本研究中,我们确定了阿托伐他汀是否可以诱导B16F10的铁下垂。卵细胞被用于治疗高胆固醇血症。为了证明这一点,我们处理了小鼠黑色素瘤细胞系B16F10。OVA用不同浓度的阿托伐他汀,从低到高,然后是24小时的培养期。在我们的实验中用阿托伐他汀治疗的组中,我们观察到与对照组相比,细胞活力的下降取决于治疗的浓度。阿托伐他汀在B16F10中的IC50值。卵圆细胞为49.89 μM。与对照组相比,阿托伐他汀治疗导致活性氧的产生和铁离子的积累呈浓度依赖性增加。此外,阿托伐他汀治疗显示出凋亡细胞数量和钙网蛋白表达的浓度依赖性增加,明显超过对照组。对凋亡相关蛋白表达水平的分析显示,与对照组相比,阿托伐他汀治疗组GPX4的表达显著降低。这些发现有力地表明,阿托伐他汀有望成为一种有效的抗癌药物,能够诱导黑色素瘤细胞中的铁下垂。
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