Acrid-release and bitter-downbearing therapy and banxia xiexin decoction regulate Wnt/β-catenin pathway, inhibit proliferation and invasion, and induce apoptosis in gastric cancer cells

OBJECTIVETo explore the efficacy of the acrid-release and bitter-downbearing therapy and Banxia Xiexin Decoction (BXD) in treating gastric cancer (GC). METHODSBXD was decocted, and serum containing medicine was prepared from rats. The SNU-16 cells were cultured with different concentrations of BXD s...

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Veröffentlicht in:American journal of translational research 2021-01, Vol.13 (6), p.6211-6220
Hauptverfasser: Sun, Xiaofen, Xue, Dewen, Zhang, Kanru, Jiang, Fang, Li, Duoqiao
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Sprache:eng
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Zusammenfassung:OBJECTIVETo explore the efficacy of the acrid-release and bitter-downbearing therapy and Banxia Xiexin Decoction (BXD) in treating gastric cancer (GC). METHODSBXD was decocted, and serum containing medicine was prepared from rats. The SNU-16 cells were cultured with different concentrations of BXD serum (25, 50, 100 μL/mL). Then, those were treated with BXD and Wnt/β-catenin pathway activator (LiCl) and divided into three groups: Control group, BXD group and BXD+LiCl group. Activation of the Wnt/β-catenin pathway was detected by immunofluorescence staining, qRT-PCR, and western blot. Cell activity, clone formation, invasion, metastasis and apoptosis in each group were examined by MTT, clone formation test, Transwell and flow cytometry. The oxidative stress measures in cells of each group were tested by an oxidative stress kit. RESULTSWith increasing BXD concentration, the clonogenic ability of cells was inhibited. BXD can inhibit cell activity, clone formation, invasion and metastasis, promote oxidative stress, and induce apoptosis. It can also inhibit the activation of Wnt/β-catenin signaling pathway. A Wnt/β-catenin signaling pathway activator could partially inhibit the action of BXD. CONCLUSIONBXD participates in GC treatment by inhibiting Wnt/β-catenin signaling pathway, thus inhibiting GC cell activity and clone formation, promoting oxidative stress, and inducing apoptosis.
ISSN:1943-8141
1943-8141