中国肿瘤生物治疗杂志2026，Vol.33Issue(3)：270-279,10.DOI:10.3872/j.issn.1007-385x.2026.03.006
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
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
摘要
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 OE-LGALS3+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 ofPPⅡ.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.关键词
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Key words
thyroid cancer(TC)/Paris polyphylla saponin Ⅱ(PP Ⅱ)/lectin-galactosidebinding-soluble(LGALS3)/malignant biological behaviors/PI3K/AKT signaling pathway分类
医药卫生引用本文复制引用
孙健玮,张燕,杜泽飞,阮小荟,郑梦扬,梁海峰..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[J].中国肿瘤生物治疗杂志,2026,33(3):270-279,10.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) （昆医联合专项）
云南省"兴滇英才"支持计划医疗卫生人才项目(XDYC-MY-2022-070) （XDYC-MY-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 （张彭跃）
云南省红河州(沙红英)院士专家工作站项目 （沙红英）
