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OA

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.