Effect of α-mangostin on proliferation,migration,invasion and tumor angiogenesis of MKN45 gastric cancer cell and its mechanisms

Ma Linwei; Xu Hongtao; Dai Xiaoli; Han Zhongbao

doi:10.13406/j.cnki.cyxb.001219

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Effect of α-mangostin on proliferation,migration,invasion and tumor angiogenesis of MKN45 gastric cancer cell and its mechanisms

更新时间：2024-01-17

- Effect of α-mangostin on proliferation,migration,invasion and tumor angiogenesis of MKN45 gastric cancer cell and its mechanisms
- Journal of Chongqing Medical University Vol. 42, Issue 11, Pages: 1426-1432(2017)
- 作者机构：
  
  盐城卫生职业技术学院临床医学教研室
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.001219
  CLC： R735.2
- Published：2017，
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Ma Linwei, Xu Hongtao, Dai Xiaoli, et al. Effect of α-mangostin on proliferation,migration,invasion and tumor angiogenesis of MKN45 gastric cancer cell and its mechanisms. [J]. Journal of Chongqing Medical University 42(11):1426-1432(2017)
DOI：

Ma Linwei, Xu Hongtao, Dai Xiaoli, et al. Effect of α-mangostin on proliferation,migration,invasion and tumor angiogenesis of MKN45 gastric cancer cell and its mechanisms. [J]. Journal of Chongqing Medical University 42(11):1426-1432(2017) DOI： 10.13406/j.cnki.cyxb.001219.

摘要

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。

Abstract

Objective:To explore the effect of α-mangostin on proliferation

migration

invasion and tumor angiogenesis of human gastric cancer cell MKN45 and its mechanisms. Methods:MTS was used to study the effect of α-mangostin on proliferation of MKN45 cells. Wound healing and Transwell experiments were used to study the effect of α-mangostin on migration and invasion of MKN45 cells in vitro

respectively. Rat arterial ring experiment was used to examine the effect of α-mangostin on tumor angiogenesis. ELISA was used to examine the effect of α-mangostin on expression of vascular endothelial growth factor（VEGF）

tumor necrosis factor-α（TNF-α）

transforming growth factor-β（TGF-β）and basic fibroblast growth factor（b FGF）to explore the potential mechanisms of α-mangostin on regulation of tumor angiogenesis. Western blot was used to detect the effect of α-mangostin on expression of MMP-2

MMP-9

N-cadherin and E-cadherin to explore the potential mechanisms of α-mangostin on regulation of tumor migration and invasion. Results:The proliferation of MKN45 cells in vitro was significant inhibited by α-mangostin compared with the control group. α-mangostin significantly inhibited the migration and invasion of MKN45 cells

respectively. Rat arterial ring experiment showed that α-mangostin inhibited the tumor angiogenesis induced by tumor cell. The protein expressions of VEGF

TNF-α

TGF-β and b FGF were significant inhibited by α-mangostin. Moreover

the expression of MMP-2

MMP-9 and N-cadherin were significant downregulated while E-cadherin was significant upregulated. Conclusion:α-mangostin has anti-proliferation

anti-migration

anti-invasion and antiangiogenesis effects on MKN45 cell

and the potential mechanisms may due to:（1）inhibits the tumor cell migration and tumor angiogenesis-related proteins expression;（2）inhibits the process of epithelial-mesenchymal transition of MKN45 cells.

关键词

α-倒捻子素胃癌细胞增殖迁移与侵袭血管生成分子机制

Keywords

α-mangostinGastric cancer cellproliferationmi gration and invasiontumor angiogensismolecular mechanisms

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