Inducing cell proliferation inhibition, apoptosis, and motility reduction by silencing long noncoding ribonucleic acid metastasis-associated lung adenocarcinoma transcript 1 in urothelial carcinoma of the bladder.

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.