In the article, we investigated the anti-
metastasis mechanism of
RY10-4, an anti-
tumor compound derived from
protoapigenone, in
breast tumor cells MB-MDA-231. The analog of
protoapigenone with an unaromatic B-ring was verified to suppress the proliferation of several
tumor cells by previous research that also showed that several
tumor progression such as inducing apoptosis and anti-angiogenesis could be acted on by
RY10-4. In the article, we investigated the mechanism about how
RY10-4 suppressed the invasion of MDA-MB-231. Firstly, the transwells assays with and without
matrigel were adapted to evaluate the anti-
metastasis and anti-invasion activity. Much research had demonstrated that the ECM and
E-cadherin/β-
catenin complex play an important role in cell adhesion and the formation of the cell skeleton, and as we knew the abnormal and absent expression of ECM and
E-cadherin/β-
catenin complex are found in many malignant cells. The result demonstrated that the amount and distribution of
E-cadherin/β-
catenin complex were backed on track by
RY10-4, and the expression of
MMP-2/9 in MDA-MB-231, which functions as a major negative factor of ECM, was down-regulated after co-cultured with
RY10-4. Furthermore the pathway related to
MMP-2/9 and
E-cadherin was assessed by the western blot. As the results showed, the MAPK pathway and the spread of β-
catenin were affected by
RY10-4 to exert the anti-
metastasis on MDA-MB-231. Collectively, the research revealed a novel anti-
tumor ability of
RY10-4 by inhibiting migration and invasion in MDA-MB-231.