藏红花素通过MTOR信号通路诱导卵巢癌HO-8910细胞自噬
Crocin Induced Autophagy through MTOR Signaling in Ovarian Cancer HO-8910 Cells
DOI: 10.12677/acm.2024.1492598, PDF,    国家自然科学基金支持
作者: 夏 丹*:山东医学高等专科学校病理教研室,山东 临沂;临沂市人民医院病理科,山东 临沂;韦志永, 刘文静, 訾 臣:临沂市人民医院病理科,山东 临沂
关键词: 藏红花素卵巢癌HO-8910细胞自噬MTORCrocin Ovarian Cancer HO-8910 Cell Autophagy MTOR
摘要: 目的:探讨藏红花素对卵巢癌HO-8910细胞自噬的影响及其分子机制。方法:用Western印迹法测定内源性LC3B-II蛋白的稳态水平以及MTOR及其下游底物的磷酸化水平。用荧光和共聚焦显微镜检测GFP-LC3B斑点的分布。结果:与对照细胞相比,用不同浓度的藏红花素处理的HO-8910细胞中内源性LC3B-II蛋白的稳态水平和GFP-LC3B斑点的分布以剂量依赖的方式增强。用藏红花素处理HO-8910细胞后,MTOR及其下游底物的磷酸化水平显著降低。结论:藏红花素通过抑制MTOR信号通路促进卵巢癌HO-8910细胞自噬体的形成。
Abstract: Aims: To investigate the mechanism through which crocin influences the autophagy of ovarian cancer HO-8910 cells. Methods: Western blotting assay was used to determine the steady-state levels of endogenous LC3B-II protein and the phosphorylation level of MTOR and its downstream substrates. Fluorescence and confocal microscopy was used to detect the distribution of GFP-LC3B puncta. Results: Compared to the control cells, the steady-state levels of endogenous LC3B-II protein and the distribution of GFP-LC3B puncta were enhanced in the HO-8910 cells treated with various concentration of crocin in a dose-dependent manner. Following treatment of HO-8910 cells with crocin, the phosphorylation level of MTOR and its downstream substrates decreased significantly. Conclusions: Crocin promotes the formation of autophagosome in ovarian cancer HO-8910 cells by inhibiting the MTOR signaling pathway.
文章引用:夏丹, 韦志永, 刘文静, 訾臣. 藏红花素通过MTOR信号通路诱导卵巢癌HO-8910细胞自噬[J]. 临床医学进展, 2024, 14(9): 1297-1306. https://doi.org/10.12677/acm.2024.1492598

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