| 曾小洁,范小雪,陈小芬,等.棕矢车菊素调节 PI3K/AKT/mTOR信号通路对肝癌细胞恶性生物学行为的影响[J].安徽医药,2025,29(11):2170-2175. |
| 棕矢车菊素调节 PI3K/AKT/mTOR信号通路对肝癌细胞恶性生物学行为的影响 |
| Effect of jaceosidin on malignant biological behavior of hepatocellular carcinoma cells through regulation of PI3K/AKT/mTOR signaling pathway |
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| DOI：10.3969/j.issn.1009-6469.2025.11.010 |
| 中文关键词: 佩兰属 黄酮类 棕矢车菊素 PI3K/AKT/mTOR信号通路 凋亡 增殖 侵袭 Hep G2细胞 |
| 英文关键词: Eupatorium Flavones Jaceosidin PI3K/AKT/mTOR signaling pathway Apoptosis Proliferation Invasion Hep G2 cells |
| 基金项目: |
| 作者 | 单位 | E-mail | | 曾小洁 | 海南医学院第一附属医院,感染科,海南海口 570100 | | | 范小雪 | 海南医学院第一附属医院,感染科,海南海口 570100 | | | 陈小芬 | 海南医学院第一附属医院,感染科,海南海口 570100 | | | 张倩倩 | 海南医学院第一附属医院,感染科,海南海口 570100 | | | 谢玉玲 | 海南医学院第一附属医院,创面修复科,海南海口 570100 | | | 邢小芳 | 海南医学院第一附属医院,感染科,海南海口 570100 | 1139506387@qq.com |
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| 中文摘要: |
| 目的探究棕矢车菊素调节磷脂酰肌醇 3激酶( PI3K)/蛋白激酶 B(AKT)/哺乳动物雷帕霉素靶蛋白( mTOR)信号通路对肝癌细胞恶性生物学行为的影响。方法 2022年 10月至 2023年 3月，使用不同浓度的棕矢车菊素( 0、5、10、20、40、80、160 μmol/L)干预人肝癌细胞 HEPG2和人正常肝细胞 HL-7702，以细胞计数试剂盒( CCK-8)法检测细胞存活率。将 HEPG2细胞分为对照组(正常培养)、棕矢车菊素低剂量组( 10 μmol/L)、棕矢车菊素中剂量组( 20 μmol/L)、棕矢车菊素高剂量组( 40 μmol/L)和 740Y-P组(40 μmol/L棕矢车菊素 +10 μmol/L PI3K/AKT/mTOR信号通路激活剂 740Y-P)各组细胞使用对应剂量的药物干预 24 h。以平板克隆法检测细胞克隆形成能力；以流式细胞术检测细胞凋亡；以 Transwell小室法，检测细胞迁移和侵袭；以蛋白质印迹法检测细胞微管相关蛋白 1轻链 3-Ⅱ/Ⅰ(LC3-Ⅱ/Ⅰ)、自噬蛋白 p62、PI3K、磷酸化( p-)PI3K、AKT、p-AKT、mTOR、p-mTOR蛋白表达。结果与 0 μmol/L［( 98.26±5.92)%］相比， 10 μmol/L［( 80.75±4.67)%］、 20 μmol/L［( 72.17±4.43)%］、 40 μmol/L［(59.52±4.05)%］、 80 μmol/L［(46.86±3.59)%］、 160 μmol/L［(31.48±2.67)%］棕矢车菊素均能呈剂量依赖性抑制 HEPG2细胞存活率( P<0.05)半抑制浓度为( 62.30±3.67)μmol/L，棕矢车菊素 5、10、20、40、80 μmol/L对 HL-7702细胞存活率的影响差异无统计学意义，后续选，取 10、20、40 μmol/L的棕矢车菊素剂量用于实验。与对照组相比，棕矢车菊素低、中、高剂量组 HEPG2细胞克隆、迁移和侵袭个数以及细胞 p62、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR蛋白表达明显降低( P<0.05)，细胞凋亡率和 LC3-Ⅱ/Ⅰ蛋白表达明显升高( P<0.05)；与棕矢车菊素高剂量组相比， 740Y-P组 HEPG2细胞克隆、迁移和侵袭个数以及细胞 p62、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR蛋白表达明显升高，细胞凋亡率和 LC3-Ⅱ/Ⅰ蛋白表达明显降低( P<0.05)。结论 棕矢车菊素可通过抑制 PI3K/AKT/mTOR信号通路抑制肝癌细胞增殖、迁移和侵袭等一系列细胞恶性生物学行为。 |
| 英文摘要: |
| Objective To investigate the effect of jaceosidin on the malignant biological behavior of hepatocellular carcinoma cellsthrough regulation of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway.Methods Between October 2022 and March 2023, human hepatocellular carcinoma cells HepG2 and human normal hepato-cytes HL-7702 were treated with different concentrations of jaceosidin (0, 5, 10, 20, 40, 80, 160 μmol/L). Cell viability was determinedusing Cell Counting Kit-8 (CCK-8) assay. HepG2 cells were divided into the following groups: control group (normal culture), low dosejaceosidin group (10 μmol/L), medium-dose jaceosidin group (20 μmol/L), high-dose jaceosidin group (40 μmol/L), and 740Y-P group (40 μmol/L jaceosidin + 10 μmol/L PI3K/AKT/mTOR signaling pathway activator 740Y-P). Cells in each group were treated with corre-sponding concentrations for 24 h. Colony formation ability was assessed by plate colony formation assay; apoptosis was detected by flowcytometry; cell migration and invasion were evaluated using Transwell assays; Western blotting was used to measure protein expression ofmicrotubule-associated protein 1 light chain 3-Ⅱ/Ⅰ (LC3-Ⅱ/Ⅰ), autophagy protein p62, PI3K, phosphorylated (p-)PI3K, AKT, p-AKT, mTOR and p-mTOR. Results Compared with 0 μmol/L [(98.26±5.92) % ], jaceosidin at 10 μmol/L [(80.75±4.67) % ], 20 μmol/L[(72.17±4.43) % ], 40 μmol/L [(59.52±4.05) % ], 80 μmol/L [(46.86±3.59) % ], 160 μmol/L [(31.48±2.67) % ] significantly inhibitedHepG2 cell viability in a dose-dependent manner (P<0.05). The half-maximal inhibitory concentration was (62.30±3.67) μmol/L. Jaceo-sidin at 5, 10, 20, 40, 80 μmol/L showed no significant effect on HL-7702 cell viability; therefore, 10, 20, and 40 μmol/L jaceosidinwere selected for subsequent experiments. Compared with the control group, the low-, medium-, and high-dose jaceosidin groupsshowed significantly reduced numbers of HepG2 cell colonies, migrations, and invasions, as well as decreased protein expression ofp62, p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR (P<0.05), while apoptosis rate and LC3-Ⅱ/Ⅰ protein expression were signifi-cantly increased (P<0.05). Compared with the high-dose jaceosidin group, the 740Y-P group exhibited significantly increased numbers ofHepG2 cell colonies, migrations, and invasions, as well as elevated protein expression of p62, p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/ mTOR, while apoptosis rate and LC3-Ⅱ/Ⅰ protein expression were significantly decreased (P<0.05).Conclusion Jaceosidin can sup-press proliferation, migration, invasion and other malignant biological behaviors of hepatocellular carcinoma cells by inhibiting thePI3K/AKT/mTOR signaling pathway. |
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