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Archive > Volume 32 Issue 6 > 2025,32(6):604-610. DOI:10.3872/j.issn.1007-385X.2025.06.006 Prev Next
Basic Research
Toxifolin inhibits malignant biological behaviors of bladder cancer T24 cells via Rac1/NF-κB/AKT signaling pathway
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Abstract:
[Abstract] Objective: To investigate the effect of toxifolin (TAX) on the malignant biological behaviors of human bladder cancer T24 cells through the Rac1/NF-κB/AKT signaling pathway. Methods: Bladder cancer T24 cells were routinely cultured and divided into: Ctrl group (untreated), TAX-L group (5 μmol/L TAX), TAX-M group (10 μmol/L TAX), TAX-H group (20 μmol/L TAX), and TAX-H+ Rac1 activator group (20 μmol/L TAX + 50 nmol/L ML-097). CCK-8 method, clone formation assay, scratch healing assay, Transwell chamber assay, and flow cytometry were used to evaluate the effects of different concentrations of TAX on the proliferation, migration, invasion, and apoptosis of T24 cells. WB method was used to examine the expression of apoptosis-related proteins, epithelial mesenchymal transition (EMT)-related proteins, and Rac1/NF-κB/AKT axis related proteins in T24 cells; A nude mice xenograft model was used to assess the effect of TAX on tumor growth. Results: TAX dose-dependently inhibited the proliferation, migration, and invasion of T24 cells and promoted apoptosis (all P < 0.05). TAX also increased the expression of apoptosis proteins BAX and E cadherin, while decreasing the expression of Bcl-2, N-cadherin, and Rac1/NF-κB/AKT signaling pathway-related proteins (all P < 0.05). Furthermore, TAX inhibited tumor growth in the xenograft model (P < 0.05). ML-097 partially reversed these effects (all P < 0.05). Conclusion: TAX inhibits the malignant biological behaviors of bladder cancer T24 cells and promotes their apoptosis by inhibiting Rac1/NF-κB/AKT signaling pathway.
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