| 郭秋生,黄鸯鸯,姜少华,吕仙梅.雷公藤内酯酮通过调控HMGB3介导的Wnt/β-catenin信号通路诱导三阴性乳腺癌细胞凋亡的机制研究[J].浙江中西医结合杂志,2025,35(12): |
| 雷公藤内酯酮通过调控HMGB3介导的Wnt/β-catenin信号通路诱导三阴性乳腺癌细胞凋亡的机制研究 |
| Mechanistic Study on Triptonide-Induced Apoptosis in Triple-Negative Breast Cancer Cells via Modulation of the HMGB3-Mediated Wnt/β-Catenin Signaling Pathway |
| 投稿时间：2025-03-18 修订日期：2025-10-26 |
| DOI： |
| 中文关键词: 三阴性乳腺癌 雷公藤内酯酮 HMGB3 Wnt/β-catenin信号通路 |
| 英文关键词:Triple Negative Breast Cancer Triptonide HMGB3 Wnt/β-catenin signaling pathway |
| 基金项目:金华市公益性技术应用研究项目（基金号：2024-4-073）。 |
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| 中文摘要: |
| 目的 研究雷公藤内酯酮(Tpn)对三阴性乳腺癌(TNBC)细胞凋亡的诱导作用及其可能的分子机制。 方法 体外培养TNBC细胞株HCC 1806,将细胞分为四组：对照组、Tpn低浓度组(10 nmol/L)、中浓度组(20 nmol/L)、高浓度组(40 nmol/L)。通过细胞增殖-毒性实验(CCK-8)、克隆形成实验和细胞迁移实验(Transwell)评估Tpn对HCC 1806细胞增殖、克隆形成和迁移能力的影响。使用流式细胞术检测Tpn对细胞凋亡的促进作用。利用Western blot分析Tpn对HCC 1806细胞中Cleaved-Caspase-3、Cleaved-PARP、HMGB3、Wnt 3a及β-catenin等蛋白的影响。通过转染HMGB3过表达质粒建立HMGB3过表达细胞株(OE-HMGB3)及对照空载体质粒细胞株(Vector),分别用Tpn处理,并通过Western blot分析Tpn对OE-HMGB3和Vector细胞株中相关蛋白的影响。 结果 Tpn能够抑制HCC 1806细胞的增殖、克隆形成和侵袭能力,并诱导细胞凋亡。这种效应与HMGB3、Wnt 3a及β-catenin蛋白表达的降低相关,而HMGB3的过表达可以抵消这些影响。 结论 Tpn能够促进HCC 1806细胞的凋亡,其机制可能通过HMGB3介导的Wnt/β-catenin信号通路实现。 |
| 英文摘要: |
| Objective To explore the apoptotic effects of triptolide (Tpn) on triple-negative breast cancer (TNBC) cells and its potential molecular mechanisms. Methods HCC 1806 TNBC cells were cultured in vitro and divided into four groups: Control, Tpn low-dose (10 nmol/L), medium-dose (20 nmol/L), and high-dose (40 nmol/L). The CCK-8, clonogenic, and Transwell assays assessed Tpn"s impact on cell proliferation, colony formation, and migration. Flow cytometry measured Tpn-induced apoptosis. Western blot analyzed Tpn"s effects on Cleaved-Caspase-3, Cleaved-PARP, HMGB3, Wnt 3a, and β-catenin proteins. HMGB3-overexpressing (OE-HMGB3) and control vector cells were established via plasmid transfection, then treated with Tpn. Western blot compared Tpn"s effects on these cells. Results Tpn inhibited HCC 1806 cell proliferation, colony formation, and invasion, while inducing apoptosis. These effects correlated with reduced HMGB3, Wnt 3a, and β-catenin expression, which were counteracted by HMGB3 overexpression. Conclusion Tpn promotes HCC 1806 cell apoptosis, likely through the HMGB3-mediated Wnt/β-catenin pathway. |
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