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目的:探讨α-倒捻子素对人胃癌细胞MKN45增殖、迁移、侵袭和血管生成的影响及其作用机制。方法:MTS法研究α-倒捻子素对人胃癌细胞MKN45增殖的影响;伤口愈合实验及Transwell实验分别用于研究α-倒捻子素对MKN45细胞体外迁移及侵袭的影响;采用大鼠动脉环实验检测α-倒捻子素对MKN45胃癌细胞血管生成的影响;ELISA实验检测α-倒捻子素对MKN45细胞分泌的血管内皮生长因子(vascular endothelial growth factor,VEGF)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、转化生长因子-β(transforming growth factor-β,TGF-β)及碱性成纤维细胞生长因子(basic fibroblast growth factor,b FGF)表达的影响等;Western blot检测α-倒捻子素对基质金属蛋白酶-2(matrix metalloproteinase-2,MMP-2)、基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)、神经-钙黏素(N-cadherin)及上皮-钙黏素(E-cadherin)蛋白表达的影响。结果:α-倒捻子素能够明显抑制人胃癌细胞MKN45的增殖,且具有剂量依赖性;α-倒捻子素能够明显抑制MKN45细胞的迁移和侵袭;动脉环实验结果显示α-倒捻子素能够抑制MKN45细胞诱导的血管生成。ELISA结果显示,α-倒捻子素能够抑制VEGF、TNF-α、TGF-β及b FGF的蛋白表达;Western blot结果显示α-倒捻子素能够下调MMP-2、MMP-9及神经-钙黏素的表达,同时上调上皮-钙黏素的表达。结论:α-倒捻子素能够抑制MKN45人胃癌细胞的增殖、迁移、侵袭和血管生成,其发挥作用可能与以下两方面机制相关:(1)抑制调控肿瘤细胞迁移及血管生成相关蛋白的表达;(2)抑制MKN45细胞的上皮间质转化。
Objective: To investigate the effects of α-mangostin on the proliferation, migration, invasion and angiogenesis of human gastric cancer cell MKN45 and its mechanism of action. METHODS: MTS assay was used to study the effects of α-mangostin on the proliferation of human gastric cancer cells MKN45. Wound healing assay and Transwell assay were used to study the effects of α-mangostin on migration and invasion of MKN45 cells in vitro. The effects of α-mangostin on angiogenesis in MKN45 gastric cancer cells were detected. The vascular endothelial growth factor (VEGF) and tumor necrosis factor-α secreted by MKN45 cells were detected by ELISA. -α, TNF-α), TGF-β and basic fibroblast growth factor (b FGF) expression; Western blot detection α - Melatonin affects matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), neuronal cadherin, and epithelial- The effect of E-cadherin protein expression. Results: α-mangostin can significantly inhibit the proliferation of human gastric cancer cell MKN45 in a dose-dependent manner. α-mangostin can significantly inhibit the migration and invasion of MKN45 cells. The results of arterial ring experiments show that α-mangostin can inhibit Induction of angiogenesis by MKN45 cells. ELISA results showed that α-mangostin can inhibit the protein expression of VEGF, TNF-α, TGF-β and b FGF; Western blot results showed that α-mangostin can down-regulate MMP-2, MMP-9 and neuro-cadherin The expression of ERK also up-regulates the expression of E-cadherin. CONCLUSION: α-mangostin can inhibit the proliferation, migration, invasion and angiogenesis of MKN45 human gastric cancer cells, and its function may be related to the following two mechanisms: (1) inhibiting the regulation of tumor cell migration and angiogenesis-related protein expression; (2) Inhibition of epithelial mesenchymal transition in MKN45 cells.