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phb2调控线粒体自噬对胶质瘤放射敏感性的影响及机制研究
首发时间：2024-04-08
摘要：目的：探究敲低phb2对胶质瘤细胞放射敏感性以及phb2调控电离辐射诱导胶质瘤细胞线粒体自噬的机制。方法：cck8实验检测胶质瘤增殖情况，流式细胞术检测细胞凋亡、细胞周期、线粒体膜电位与细胞内超氧化物水平，免疫荧光检测phb2与lc3b共定位情况，克隆实验检测细胞放射敏感性，蛋白质电泳检测线粒体自噬相关蛋白parl、pgam5、pink1表达变化。结果：常氧或乏氧条件下，敲低phb2抑制胶质瘤细胞增殖、促进细胞凋亡、阻滞细胞周期在g2/m期，增强胶质瘤细胞放射敏感性。敲低phb2抑制线粒体膜电位下降，促进线粒体超氧化累积，抑制lc3b与phb2在线粒体上结合。电离辐射促进parl与phb2结合，敲低phb2抑制pgam5、pink1表达，上调tom20表达。结论：电离辐射诱导胶质瘤细胞发生线粒体自噬，敲低phb2增强常氧或乏氧胶质瘤细胞放射敏感性，上调胶质瘤细胞凋亡率，加重线粒体损伤。phb2调控电离辐射诱导线粒体自噬可能与parl-pgam5-pink1通路有关。
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the effect of phb2-regulated mitophagy on the radiosensitivity of glioma cells and its mechanism research
abstract：objective: to explore the effect of phb2 knockdown on radiosensitivity of glioma cells and the mechanisms of phb2-regulated ionizing radiation-induced mitophagy. methods: the proliferation of gliomas was detected by cck8 assay. apoptosis, cell cycle, mitochondrial membrane potential and mitochondrial superoxide levels were detected by flow cytometry. the co-localization of phb2 and lc3b was detected by immunofluorescence, and the radiosensitivity of gliomas was detected by cloning assay. the expression changes of mitophagy related proteins parl, pgam5 and pink1 were detected by western blot. result：under normoxic or hypoxic culture conditions, knockdown of phb2 inhibited proliferation of glioma cells, promoted apoptosis, blocked cell cycle at g2/m, and enhanced radiosensitivity of glioma cells. knockdown of phb2 inhibited mitochondrial membrane potential decline, promoted mitosox accumulation and inhibited lc3b binding to mitochondria. ionizing radiation promoted parl binding to phb2, as well as knockdown of phb2 inhibited pgam5 and pink1 expression, and upregulated tom20 expression. conclusion：ionizing radiation induced mitophagy in glioma cells. knockdown of phb2 enhanced radiosensitivity, upregulated apoptosis rate in glioma cells. phb2 regulated ionizing radiation-induced mitophagy in glioma cells, which may be related to parl-pgam5-pink1 pathway.
keywords： radiosensitivity phb2 mitophagy gbm
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phb2调控线粒体自噬对胶质瘤放射敏感性的影响及机制研究
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