OBJECTIVE: To study the expression patterns of long noncoding ribonucleic acid 
(RNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and the 
cell proliferation inhibition, apoptosis, and motility changes induced by 
silencing MALAT1 in urothelial carcinoma of the bladder.
MATERIALS AND METHODS: The expression levels of MALAT1 were determined using 
real-time quantitative polymerase chain reaction in cancerous tissues and paired 
normal tissues in a total of 36 patients with urothelial carcinoma of the 
bladder. Expression differences were analyzed according to the grade and stage. 
Bladder urothelial carcinoma T24 and 5637 cells were transfected with MALAT1 
small interfering RNA or negative control small interfering RNA. The cell 
proliferation changes of the transfected bladder urothelial carcinoma cells were 
determined using the MTT assay. Apoptosis caused by silencing MALAT1 was 
evaluated using the flow cytometry assay and enzyme-linked immunosorbent assay. 
The motility changes induced by silencing MALAT1 were measured using the wound 
healing assay.
RESULTS: MALAT1 was upregulated in bladder urothelial carcinoma compared with 
matched normal urothelium (P=.008). The MALAT1 expression levels were greater in 
high-grade carcinomas than in low-grade carcinoma (P=.001). The MALAT1 
expression levels were greater in invasive carcinoma than in noninvasive 
carcinoma (P=.018). Cell proliferation inhibition, increased apoptosis, and 
decreased motility were observed in MALAT1 small interfering RNA-transfected 
bladder urothelial carcinoma T24 and 5637 cells.
CONCLUSION: MALAT1 plays an oncogenic role in urothelial carcinoma of the 
bladder. Silencing MALAT1 is a potential novel therapeutic approach for this 
cancer.