HSP27 protects against ferroptosis of glioblastoma cells
HSP27 protects against ferroptosis of glioblastoma cells
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DOI：
10.1007/s13577-021-00645-6
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发表时间：
2021-11
期刊：
影响因子：
4.3
通讯作者：
Fan-En Yuan;Qian Sun;Si Zhang;Liguo Ye;Yang Xu;Zhou Xu;Baohui Liu;Shenqi Zhang;Qianxue Chen
中科院分区：
文献类型：
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作者：
Fan-En Yuan;Qian Sun;Si Zhang;Liguo Ye;Yang Xu;Zhou Xu;Baohui Liu;Shenqi Zhang;Qianxue Chen
铁死亡作为一种新形式的非凋亡调节细胞死亡，在人类癌症中发挥着重要作用。尽管有报道称HSP27是癌症中铁死亡的新型调节因子，但HSP27如何影响神经胶质瘤中的铁死亡仍不清楚。在这项研究中，我们检测了 HSP27 对胶质母细胞瘤铁死亡的影响。 HSP27 过表达可保护胶质母细胞瘤细胞免遭erastin 诱导的铁死亡，而HSP27 耗竭则促进erastin 诱导的胶质母细胞瘤铁死亡。值得注意的是，HSP27 磷酸化是 HSP27 在erastin 诱导的铁死亡中发挥保护功能所必需的。总体而言，我们的研究揭示了神经胶质瘤中铁死亡的新分子机制，并确定 HSP27 是铁死亡的负调节因子和神经胶质瘤治疗的潜在靶点。
Ferroptosis, as an new form of non-apoptotic regulated cell death, plays an important role in human cancers. Although it is reported that HSP27 is an novel regulator of ferroptosis in cancer, it remains unknown how HSP27 affects ferroptosis in glioma. In this study, we examined the effect of HSP27 on the ferroptosis of glioblasotma. HSP27 overexpression protects glioblastoma cells from erastin-induced ferroptosis while HSP27 depletion promotes erastin-induced ferroptosis of glioblastoma. Notably, HSP27 phosphorylation is required for the protective function of HSP27 in erastin-induced ferroptosis. Overall, our study reveal novel molecular mechanisms of ferroptosis in glioma and also identify HSP27 as a negative regulator of ferroptosis and a potential target for the treatment of glioma.