[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 ），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。

[Abstract] Objective: To investigate the molecular mechanisms by which Paris polyphyllaa saponin (PPⅡ) suppresses the malignant biological behaviors of thyroid cancer (TC). Methods: Thyroid cancer TPC1 cells were routinely cultured and divided into five experimental groups, designated as sh-NC, sh-lectin-galactoside binding-soluble 3 (sh-LGALS3), OE-NC, OE-LGALS3, and OELGALS3 + PPⅡ. TPC1 cells in each group were transfected with corresponding plasmids using transfection reagents.qPCR was used to detect the expression of LGALS3 mRNA in TPC1 cells. WB was performed to examine the expression of LGALS3 and PI3K/AKT signaling pathway-related proteins. CCK-8 assay, Transwell assay, wound healing assay, and flow cytometry were used to assess the proliferation, migration, invasion, and apoptosis of TPC1 cells in each group. Results: PPⅡ significantly inhibited the proliferation, migration, and invasion of TPC1 cells, while inducing apoptosis (all P < 0.000 1). Database analyses revealed that LGALS3 was highly expressed in thyroid cancer tissues (P < 0.001) and was identified as a potential target gene of PPⅡ. LGALS3 was highly expressed in TPC1 cells (P < 0.000 1). Knockdown of LGALS3 suppressed the malignant biological behaviors of TPC1 cells and promoted apoptosis (all P < 0.000 1). PPⅡ inhibited the malignant biological behaviors of TPC1 cells by downregulating LGALS3 mRNA and protein expression (P < 0.01 or P < 0.001). Furthermore, PP Ⅱ suppressed the activation of the PI3K/AKT signaling pathway by inhibiting LGALS3 expression (P < 0.001 or P < 0.000 1). LGALS3 promoted the malignant biological behaviors of TPC1 cells through the PI3K/AKT signaling pathway (P < 0.000 1). Conclusion: PPⅡ exerts anti-tumor effects in thyroid cancer by inhibiting LGALS3 expression in TPC1 cells and attenuating the overactivation of the PI3K/AKT signaling pathway.

[基金项目] 云南省科技厅应用基础研究重点项目（昆医联合专项）（202301AY070001-037）；云南省“兴滇英才”支持计划医疗卫生人才项目（XDYCMY-2022-070）；中国健康促进基金会公立医院高质量发展科研基金重点项目；云南省（张彭跃）专家基层科研工作职责项目； 云南省红河州（沙红英）院士专家工作站项目