Glucosamine induces autophagic cell death through the stimulation of ER stress in human glioma cancer cells
Glucosamine induces autophagic cell death through the stimulation of ER stress in human glioma cancer cells
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DOI：
10.1016/j.bbrc.2010.07.050
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发表时间：
2010-08-13
影响因子：
3.1
通讯作者：
Baek, Won-Ki
中科院分区：
文献类型：
--
作者：
Hwang, Mi-Sun;Baek, Won-Ki
自噬可以促进细胞存活或死亡，但其在癌症中双重作用的分子基础还不清楚。在这里，我们报告，葡萄糖胺诱导自噬细胞死亡，通过刺激内质网（ER）的压力在U87 MG人胶质瘤癌细胞。用葡糖胺处理降低了细胞活力并增加了LC 3 II和GFP-LC 3荧光斑点的表达，这是自噬性细胞死亡的指示。葡糖胺介导的抑制细胞活力逆转治疗与自噬抑制剂，3-MA，和干扰RNA对Atg 5。葡糖胺诱导的ER应激表现为诱导BiP、IRE 1 α和磷酸化eIF 2 α表达。化学伴侣4-PBA降低ER应激，从而抑制葡糖胺诱导的自噬细胞死亡。总之，我们的数据表明，葡萄糖胺诱导自噬细胞死亡诱导ER应激在U87 MG胶质瘤癌细胞，并提供了新的见解的潜在抗癌特性的葡萄糖胺。(C)2010年爱思唯尔公司All rights reserved.
Autophagy can promote cell survival or death, but the molecular basis of its dual role in cancer is not well understood. Here, we report that glucosamine induces autophagic cell death through the stimulation of endoplasmic reticulum (ER) stress in U87MG human glioma cancer cells. Treatment with glucosamine reduced cell viability and increased the expression of LC3 II and GFP-LC3 fluorescence puncta, which are indicative of autophagic cell death. The glucosamine-mediated suppression of cell viability was reversed by treatment with an autophagy inhibitor, 3-MA, and interfering RNA against Atg5. Glucosamine-induced ER stress was manifested by the induction of BiP, IRE1 alpha, and phospho-eIF2 alpha expression. Chemical chaperon 4-PBA reduced ER stress and thereby inhibited glucosamine-induced autophagic cell death. Taken together, our data suggest that glucosamine induces autophagic cell death by inducing ER stress in U87MG glioma cancer cells and provide new insight into the potential anticancer properties of glucosamine. (C) 2010 Elsevier Inc. All rights reserved.