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首页> 外文期刊>Cell biology international. >p62/SQSTM1 is involved in caspase-8 associated cell death induced by proteasome inhibitor MG132 in U87MG cells
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p62/SQSTM1 is involved in caspase-8 associated cell death induced by proteasome inhibitor MG132 in U87MG cells

机译：p62 / SQSTM1参与U87MG细胞中蛋白酶体抑制剂MG132诱导的caspase-8相关细胞死亡

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摘要

Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer. Proteasome inhibitors are emerging as a new class of anti-glioma agents; however, the mechanisms of their killing malignant cells are still unclear. We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.To explore the role of autophagy and p62/SQSTM1 in MG132-induced cancer cell death, we measured the alteration of MG132's cytotoxicity by autophagy inhibition, autophagy induction or variation of p62/SQSTM1 gene expression. Autophagy was activated upon MG132 treatment for short periods, while inhibition of autophagy aggravated MG132-induced cell death followed by high levels of p62/SQSTM1 and active caspase-8 (p18). Moreover, U87MG cell death was dependent on p62/SQSTM1, and its function required its C-terminus UBA domain to attenuate the MG132-induced cell death. The results suggest that p62/SQSTM1 is a potential contributor in determining the fate of U87MG cells deficient in proteolytic activity.
机译：多形胶质母细胞瘤（GBM）是最常见和致命的脑癌类型。蛋白酶体抑制剂正在作为一类新的抗神经胶质瘤药物出现。然而，其杀死恶性细胞的机制仍不清楚。我们用蛋白酶体抑制剂MG132处理U87MG细胞，发现细胞死亡与caspase-8激活和自噬蛋白p62 / SQSTM1相关。为探讨自噬和p62 / SQSTM1在MG132诱导的癌细胞死亡中的作用，我们测量了MG132通过自噬抑制，自噬诱导或p62 / SQSTM1基因表达变化的细胞毒性。自噬在短时间内被MG132处理后被激活，而自噬的抑制加剧了MG132诱导的细胞死亡，继之以高水平的p62 / SQSTM1和活性caspase-8（p18）。此外，U87MG细胞死亡取决于p62 / SQSTM1，其功能需要其C末端UBA结构域来减弱MG132诱导的细胞死亡。结果表明，p62 / SQSTM1是确定蛋白水解活性不足的U87MG细胞命运的潜在因素。

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