HER-2 promotes breast cancer cell epithelial-mesenchymal transition by regulating ZEB1

侯　净; 任智晶; 魏　娜

doi:10.19401/j.cnki.1007-3639.2016.12.002

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HER-2 promotes breast cancer cell epithelial-mesenchymal transition by regulating ZEB1

更新时间：2025-12-31

- HER-2 promotes breast cancer cell epithelial-mesenchymal transition by regulating ZEB1
- China Oncology Vol. 26, Issue 12, Pages: 968-973(2016)
- 作者机构：
  
  1. 贵州省人民医院乳腺外科,贵州,贵阳,550002
  2. 复旦大学附属肿瘤医院放疗科，复旦大学上海医学院肿瘤学系,上海,200032
  3. 贵州省人民医院检验科,贵州,贵阳,550002
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2016.12.002
  CLC：
- Published Online：23 January 2017，
  
  Published：23 January 2016
- 稿件说明：
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侯　净,任智晶,魏　娜,等. HER-2通过ZEB1促进乳腺癌细胞上皮间质转化[J]. 中国癌症杂志, 2016, 26(12): 968-973.

侯　净, 任智晶, 魏　娜. HER-2 promotes breast cancer cell epithelial-mesenchymal transition by regulating ZEB1[J]. China Oncology, 2016, 26(12): 968-973.
侯　净,任智晶,魏　娜,等. HER-2通过ZEB1促进乳腺癌细胞上皮间质转化[J]. 中国癌症杂志, 2016, 26(12): 968-973. DOI： 10.19401/j.cnki.1007-3639.2016.12.002.

侯　净, 任智晶, 魏　娜. HER-2 promotes breast cancer cell epithelial-mesenchymal transition by regulating ZEB1[J]. China Oncology, 2016, 26(12): 968-973. DOI： 10.19401/j.cnki.1007-3639.2016.12.002.

摘要

背景与目的：人类表皮生长因子受体2(human epidermal growth factor receptor-2，HER-2)是表皮生长因子受体家族中的一员，它参与细胞多个生物过程，如细胞增殖、侵袭和凋亡等。有研究表明，HER-2与细胞上皮间质转化(epithelial-mesenchymal transition，EMT)过程相关，但具体机制有待进一步探讨，本研究旨在探讨HER-2对EMT的调节机制。方法：用Transwell小室模拟细胞的迁徙侵袭能力；采用实时荧光定量聚合酶链反应(real-time fluorescent quantitative polymerase chain reaction，RTFQ-PCR)检测目的基因的表达；用活性氧检测试剂盒检测细胞活性氧的水平。结果：Transwell小室模拟实验发现，HER-2过表达能促进乳腺癌细胞的侵袭转移；机制研究表明，HER-2能上调ZEB1，用siRNA降低ZEB1表达使HER-2过表达细胞的侵袭能力受损；此外，HER-2过表达乳腺癌细胞中活性氧水平较低。结论：HER-2可以上调ZEB1的表达而赋予乳腺癌细胞EMT相关特性，ZEB1可作为进一步研究HER-2与EMT调节关系的靶点。

Abstract

Background and purpose: Human epidermal growth factor receptor-2 (HER-2)

a member of epidermal growth factor receptor family

initiates a diverse set of signaling pathways that ultimately affect such fundamental processes as cell proliferation

cell motility and cell apoptosis. It is reported that HER-2 was associated with epithelial-mesenchymal transition (EMT) process. However

the mechanism needs further investigation. The purpose of this study was to investigate the mechanism of HER-2 on regulating EMT process. Methods: Transwell assay was used to determine the motility of breast cancer cells; Real-time fluorescence quantitative polymerase chain reaction (RTFQ- PCR) was employed to determine the expression of genes of interest

and reactive oxygen species production was measured by reactive oxygen species detection kit. Results: HER-2 overexpression in breast cancer cells could promote cell migration and invasion. Mechanistic study showed that HER-2 overexpression could upregulate ZEB1 expression. ZEB1 silencing by siRNA reduced cell motility of HER-2-overexpressing breast cancer cells. Furthermore

reactive oxygen species produced in HER-2-overexpressing breast cancer cells were less than those produced in corresponding control cells. Conclusion: Our study demonstrated that HER-2 overexpression endowed breast cancer cells with EMT related properties by upregulating ZEB1 expression. ZEB1 could be a candidate target for further study of the relationship between HER-2 and EMT.

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复旦大学附属肿瘤医院检验科，复旦大学上海医学院肿瘤学系

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Department of Breast Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital& Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College

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