Recent studies reveal that long non-coding RNAs (lncRNAs) have been shown to 
have important regulatory roles in cancer biology, and lncRNA MALAT-1 expression 
is upregulated in some tumors. However, the contributions of MALAT-1 to bladder 
cancer metastasis remain largely unknown. In the present study we evaluated 
MALAT-1 expression in bladder cancer tissues by real-time PCR, and defined its 
biological functions. We verified that MALAT-1 levels were upregulated in 
bladder cancer tissues compared with adjacent normal tissues, and MALAT-1 
expression was remarkably increased in primary tumors that subsequently 
metastasized, when compared to those primary tumors that did not metastasize. 
SiRNA-mediated MALAT-1 silencing impaired in vitro bladder cancer cell 
migration. Downregulation of MALAT-1 resulted in a decrease of the 
epithelial-mesenchymal transition (EMT)-associated ZEB1, ZEB2 and Slug levels, 
and an increase of E-cadherin levels. We further demonstrated that MALAT-1 
promoted EMT by activating Wnt signaling in vitro. These data suggest an 
important role for MALAT-1 in regulating metastasis of bladder cancer and the 
potential application of MALAT-1 in bladder cancer therapy.