Background: Coptisine, an isoquinoline alkaloid extracted from Coptidis rhizoma, has many biologicalactivities such as antidiabetic, antimicrobial and antiviral actions. However, whether coptisine exerts anti-cancermetastasis effects remains unknown. Materials and
Methods: Effects of coptisine on highly metastatic humanbreast cancer cell MDA-MB-231 proliferation were evaluated by trypan blue assay and on cell adhesion, migrationand invasion by gelatin adhesion, wound-healing and matrigel invasion chamber assays, respectively. Expressionof two matrix metalloproteinases (MMPs), MMP-9, MMP-2 and their specific inhibitors tissue inhibitor ofmetalloproteinase 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, andinvasion through the matrigel in MDA-MB-231 breast cancer cells. RT-PCR revealed that coptisine reduced theexpression of the ECM degradation-associated gene MMP-9 at the mRNA level, and the expression of TIMP-1was up-regulated in MDA-MB-231 cells, while the expression of MMP-2 and its specific inhibitor TIMP-2 wasnot affected.
Conclusions: Taken together, our data showed that coptisine suppressed adhesion, migration andinvasion of MDA-MB-231 breast cancer cells in vitro, the down-regulation of MMP-9 in combination with theincrease of TIMP-1 possibly contributing to the anti-metastatic function. Coptisine might be a potential drugcandidate for breast cancer therapy.