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首页> 外文期刊>Journal of biochemical and molecular toxicology >4-O-methylascochlorin activates autophagy by activating AMPK and suppressing c-Myc in glioblastoma
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4-O-methylascochlorin activates autophagy by activating AMPK and suppressing c-Myc in glioblastoma

机译：4-O-甲基蔗糖通过激活AMPK和抑制胶质母细胞瘤中的C-MYC来激活自噬

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摘要

A prior study identified that 4-O-methylascochlorin (MAC), a methylated derivative of ascochlorin (ASC) from the fungus Ascochyta viciae, activates autophagy in leukemia cells by suppressing c-Myc phosphorylation. However, the effects of MAC on autophagy in other cancer cells remain unknown. In the present study, we demonstrated that MAC activated autophagy in human glioblastoma. MAC increased expression of autophagy-related proteins, such as LC3-II and Beclin-1. Moreover, MAC stimulated AMP-activated protein kinase (AMPK) phosphorylation and suppressed phosphorylation of the mTOR, p70S6K, and 4EBP1. The well-known AMPK activator metformin increased LC3-II levels, which were augmented by MAC cotreatment. AMPK knockdown decreased LC3-II levels and inhibited MAC activation of autophagy. Furthermore, MAC suppression of c-Myc expression activated autophagy. Treatment with the c-MYC inhibitor, 10058-FA, induced autophagy, as did c-Myc small interfering RNA knockdown. These effects were augmented by MAC cotreatment. Taken together, these findings indicated that MAC induces autophagy in human glioblastoma by activating AMPK signaling and inhibiting c-Myc protein expression in human glioblastoma.
机译：此前的一项研究发现，4-O-甲基抗坏血酸（MAC）是一种抗坏血酸（ASC）的甲基化衍生物，来自真菌Ascochyta viciae，通过抑制c-Myc磷酸化激活白血病细胞中的自噬。然而，MAC对其他癌细胞自噬的影响尚不清楚。在目前的研究中，我们证明MAC激活了人胶质母细胞瘤中的自噬。MAC增加自噬相关蛋白的表达，如LC3-II和Beclin-1。此外，MAC刺激AMP活化蛋白激酶（AMPK）磷酸化并抑制mTOR、p70S6K和4EBP1的磷酸化。众所周知的AMPK激活剂二甲双胍可提高LC3-II水平，MAC联合治疗可提高LC3-II水平。AMPK敲除降低LC3-II水平，抑制自噬的MAC激活。此外，MAC对c-Myc表达的抑制激活了自噬。用c-MYC抑制剂10058-FA治疗可诱导自噬，c-MYC小干扰RNA敲除也可诱导自噬。MAC协同处理增强了这些效应。综上所述，这些发现表明MAC通过激活AMPK信号和抑制人脑胶质母细胞瘤中的c-Myc蛋白表达，在人脑胶质母细胞瘤中诱导自噬。

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