Expression of E-cadherin, a hallmark of epithelial-mesenchymal transition (EMT), 
is often lost due to promoter DNA methylation in basal-like breast cancer 
(BLBC), which contributes to the metastatic advantage of this disease; however, 
the underlying mechanism remains unclear. Here, we identified that Snail 
interacted with Suv39H1 (suppressor of variegation 3-9 homolog 1), a major 
methyltransferase responsible for H3K9me3 that intimately links to DNA 
methylation. We demonstrated that the SNAG domain of Snail and the SET domain of 
Suv39H1 were required for their mutual interactions. We found that H3K9me3 and 
DNA methylation on the E-cadherin promoter were higher in BLBC cell lines. We 
showed that Snail interacted with Suv39H1 and recruited it to the E-cadherin 
promoter for transcriptional repression. Knockdown of Suv39H1 restored 
E-cadherin expression by blocking H3K9me3 and DNA methylation and resulted in 
the inhibition of cell migration, invasion and metastasis of BLBC. Our study not 
only reveals a critical mechanism underlying the epigenetic regulation of EMT, 
but also paves a way for the development of new treatment strategies against 
this disease.