自噬在神经胶质瘤放化疗中的作用及其分子调控机制研究进展

被引:3
作者
李君 [1 ,2 ]
龙林梅 [1 ]
雷陈 [3 ]
梁中琴 [1 ,2 ]
机构
[1] 苏州大学医学部药理学教研室
[2] 苏州大学医学部神经科学研究所
[3] 苏州大学医学部生物化学与分子生物学教研室
关键词
自噬; 神经胶质瘤; 抗肿瘤联合化疗方案;
D O I
暂无
中图分类号
R739.4 [神经系肿瘤];
学科分类号
100115 [医学神经生物学];
摘要
自噬是真核细胞中广泛存在的降解和再循环系统,近年研究发现,放疗和化疗不仅可引起神经胶质瘤细胞凋亡,还可以诱导自噬。细胞自噬可能导致细胞自噬死亡,也有可能导致自噬保护,显示双重效应,可见自噬与神经胶质瘤的发生、发展以及治疗密切相关。其分子调控机制可能与雷帕霉素靶蛋白,beclin 1,磷脂酰肌醇-3-激酶,第10号染色体丢失的张力蛋白同源的磷酸酶以及微管相关蛋白1轻链3等内容有关。
引用
收藏
页码:106 / 109
页数:4
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