Mechanism study on regulation of the LGALS3/PI3K/AKT signaling pathway by Paris polyphylla saponin Ⅱ in inhibiting the malignant biological behaviors of thyroid cancer cells
DOI：10.3872/j.issn.1007-385x.2026.03.006
- VernacularTitle:重楼皂苷Ⅱ调控LGALS3/PI3K/AKT信号通路抑制甲状腺癌细胞的恶性生物学行为
- Author:
SUN Jianwei1
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ZHANG Yan2
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DU Zefei3
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RUAN Xiaohui4
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ZHENG Mengyang1
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LIANG Haifeng2
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Author Information
1. Department of Ultrasound Medicine, Fifth Affiliated Hospital of Kunming Medical University, Gejiu 661000, Yunnan, China;
2. Department of Oncology, Fifth Affiliated Hospital of Kunming Medical University, Gejiu 661000, Yunnan, China;
3. Department of Pharmacy, Fifth Affiliated Hospital of Kunming Medical University, Gejiu 661000, Yunnan, China;
4. Department of Endocrinology and Metabolism, Fifth Affiliated Hospital of Kunming Medical University, Gejiu 661000, Yunnan, China
- Publication Type:Journal Article
- Keywords:
甲状腺癌；重楼皂苷Ⅱ；半乳糖凝集素3；恶性生物学行为；PI3K/AKT信号通路
- From:
Chinese Journal of Cancer Biotherapy
2026;33(3):270-279
- CountryChina
- Language:Chinese
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Abstract:
[摘 要] 目的：探究重楼皂苷Ⅱ（PPⅡ）抑制甲状腺癌（TC）恶性生物学行为的分子机制。方法：常规培养甲状腺癌细胞TPC1，实验分为sh-NC、sh-可溶性半乳糖凝集素3（sh-LGALS3）、OE-NC、OE-LGALS3和 OE-LGALS3 + PPⅡ组，用转染试剂将应用质粒转染至各组TPC1细胞中。qPCR法检测TPC1细胞中LGALS3 mRNA的表达，WB法检测各组TPC1细胞中LGALS3、PI3K/AKT信号通路相关蛋白的表达，CCK-8法、Transwell实验、划痕愈合实验和流式细胞术分别检测各组TPC1细胞增殖、迁移和侵袭能力，以及细胞凋亡情况。结果：PPⅡ抑制TPC1细胞的增殖、迁移和侵袭，并诱导其凋亡（均P < 0.000 1）。数据库数据分析显示LGALS3在甲状腺癌组织中高表达（P < 0.001）且是PPⅡ的靶基因。LGALS1在TPC1细胞中呈高表达（P < 0.000 1），敲减LGALS3抑制TPC1细胞的恶性生物学行为，并促进其凋亡（均P < 0.000 1），PPⅡ通过抑制LGALS3 mRNA和蛋白的表达（P < 0.01或P < 0.001）从而抑制TPC1细胞的恶性生物学行为（P < 0.01或P < 0.000 1），PPⅡ抑制LGALS3表达抑制PI3K/AKT信号通路的激活水平（P <0.001或P <0.000 1），LGALS3通过PI3K/AKT信号通路促进TPC1细胞的恶性生物行为（P < 0.000 1）。结论：PPⅡ通过抑制TPC1细胞中LGALS3的表达，缓解PI3K/AKT信号通路的过度激活从而发挥抑癌作用。
