Impacts of Formononetin on the Proliferation, Invasion, and Epithelial-Mesenchymal Transition of Gallbladder Cancer Cells by Inhibiting the TLR4/NF-κB Pathway
REN Yi, WU Biao*
The purpose of this study was to explore the impacts of FMNT (formononetin) on the proliferation, invasion, and EMT (epithelial-mesenchymal transition) of gallbladder cancer cells by inhibiting the TLR4 (Toll-like receptor 4)/NF-κB (nuclear factor kappa B) signaling pathway. GBC-SD gallbladder cancer cells were assigned into control group, low concentration FMNT group, medium concentration FMNT group, high concentration FMNT group, and FMNT+lipopolysaccharide group. CCK-8 was used to measure cell proliferation. The wound healing experiment was used to detect cell migration. Transwell chamber was used to evaluate cell invasion. Annexin V-FITC staining was used to detect cell apoptosis. In addition, Western blot was used to detect the expression of E-cadherin, Vimentin, TLR4, and NF-κB proteins in cells. The results showed that compared with the control group, the D value, colony formation rate, wound healing rate, number of invasive cells, Vimentin, TLR4, and NF-κB protein expression levels of GBC-SD cells in the low concentration FMNT group, medium concentration FMNT group and high concentration FMNT group decreased, while the apoptosis rate and E-cadherin protein expression level increased (P<0.05). The higher the FMNT concentration, the more significant the changes (P<0.05). Compared with the high concentration FMNT group, the D value, colony formation rate, wound healing rate, number of invasive cells, Vimentin, TLR4, and NF-κB protein expression levels of GBC-SD cells in FMNT+lipopolysaccharide group increased, while the apoptosis rate and E-cadherin protein expression level decreased (P<0.05). It is concluded that FMNT inhibits proliferation, invasion, and EMT of gallbladder cancer cells by inhibiting the TLR4/NF-κB pathway.
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