基础医学与临床 ›› 2016, Vol. 36 ›› Issue (8): 1062-1067.

• 研究论文 • 上一篇    下一篇

铁对三阴性乳腺癌细胞体外血管生成拟态的影响

张强1,史云湘2,史杪1,崔永峰1,冯琼3,王强1,和彦苓4   

  1. 1. 军事医学科学院
    2. 内蒙古科技大学包头医学院
    3. 内蒙古科技大学-包头医学院
    4. 包头医学院
  • 收稿日期:2015-01-12 修回日期:2015-11-04 出版日期:2016-08-05 发布日期:2016-07-13
  • 通讯作者: 王强 E-mail:wang76qiang@163.com
  • 基金资助:
    紧密连接蛋白及其磷酸化修饰在三阴性乳腺癌血管生成拟态中的作用;铁蛋白在雌激素诱导乳腺癌过程中的作用及机制研究

Effect of iron on the vasculogenic mimicry in triple negative breast cancer cells in vitro

  • Received:2015-01-12 Revised:2015-11-04 Online:2016-08-05 Published:2016-07-13

摘要: 目的 研究铁对三阴性乳腺癌细胞体外血管生成拟态(VM)的影响及其机制。方法 将细胞分为6组:对照组、30和300 μmol/L含羞草氨酸组、500 μmol/L去铁胺组及50和500 μmol/L乳酸亚铁组。用MTT法检测细胞增殖活力,三维培养和PAS染色鉴定细胞形成VM的能力,免疫荧光染色法检测ROS变化,Western blot检测p-ERK1/2表达。结果 去铁胺、含羞草氨酸均可显著抑制血管样结构形成(P<0.05),乳酸亚铁可促进其形成(P<0.05),并且血管样结构表现为PAS染色阳性。细胞血管样结构形成能力与胞内ROS及p-ERK1/2表达水平变化相一致。加入PD98059可以显著抑制其形成(P<0.05)。结论 铁诱导生成ROS促进VM的形成,ERK1/2的异常激活可能是主要调节机制。

关键词: 关键词:铁, 乳腺癌细胞, 血管生成拟态, p-ERK1/2

Abstract: Objective: To study the effect and possible mechanism of iron induced vasculogenic mimicry (VM) formation in breast cancer cell. Methods: We devided MDA-MB-231 cells into seven groups: control group, 500μmol/L DFO group, 300μmol/L and 30μmol/L mimosine group, 50μmol/L and 500μmol/L ferrous lactate group. MTT was used to observe the proliferation of breast cancer cell. Formation of VM was identified by both 3D culture and PAS stain method. Change of ROS in cells was measured by immunofluoresence staining method. Under difference concentrations of iron, the expression of p-ERK1/2 in MDA-MB-231 was tested by Western blot. Results: Pipeline structure was obviously inhibited in vitro in DFO- and mimosine-treated groups(P<0.05), while ferrous lactate promoted the formation of vessel-like structure(P<0.05). PAS staining demonstated that vessel-like structure was VM. Immunofluoresence staining and Western blot showed that ROS in cells were consistent with the expression of p-ERK1/2. Specific inhibitor (PD98059) significantly decreased the formation of VM(P<0.05). Conclusions: ROS is positively involved in iron-induced VM formation. Abnormal activation of ERK1/2 pathway may be the principal mechanism of regulation of ROS.

Key words: Key Word: iron, tripe-negative breast cancer cell, vasculigenice mimicry, p-ERK1/2.

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