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Suppression of Human Breast Cancer Cell Metastasis by Coptisine in Vitro

  • Li, Jing (Wuxi Higher Health Vocational Technology School, Wuxi, Jiangsu Province) ;
  • Qiu, Dong-Min (Wuxi Higher Health Vocational Technology School, Wuxi, Jiangsu Province) ;
  • Chen, Shao-Hua (Wuxi Higher Health Vocational Technology School, Wuxi, Jiangsu Province) ;
  • Cao, Su-Ping (Wuxi Higher Health Vocational Technology School, Wuxi, Jiangsu Province) ;
  • Xia, Xue-Lan (Wuxi Higher Health Vocational Technology School, Wuxi, Jiangsu Province)
  • Published : 2014.07.30

Abstract

Background: Coptisine, an isoquinoline alkaloid extracted from Coptidis rhizoma, has many biological activities such as antidiabetic, antimicrobial and antiviral actions. However, whether coptisine exerts anti-cancer metastasis effects remains unknown. Materials and Methods: Effects of coptisine on highly metastatic human breast cancer cell MDA-MB-231 proliferation were evaluated by trypan blue assay and on cell adhesion, migration and invasion by gelatin adhesion, wound-healing and matrigel invasion chamber assays, respectively. Expression of two matrix metalloproteinases (MMPs), MMP-9, MMP-2 and their specific inhibitors tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) were analyzed by RT-PCR. Results: Coptisine obviously inhibited adhesion to an ECM-coated substrate, wound healing migration, and invasion through the matrigel in MDA-MB-231 breast cancer cells. RT-PCR revealed that coptisine reduced the expression of the ECM degradation-associated gene MMP-9 at the mRNA level, and the expression of TIMP-1 was upregulated in MDA-MB-231 cells, while the expression of MMP-2 and its specific inhibitor TIMP-2 was not affected. Conclusions: Taken together, our data showed that coptisine suppressed adhesion, migration and invasion of MDA-MB-231 breast cancer cells in vitro, the down-regulation of MMP-9 in combination with the increase of TIMP-1 possibly contributing to the anti-metastatic function. Coptisine might be a potential drug candidate for breast cancer therapy.

Keywords

References

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