Knockdown of Long Non-coding RNA UCA1 Represses Gallbladder Cancer Advancement by Regulating SPOCK1 Expression via Sponging miR-613

OBJECTIVE : Patients with advanced gallbladder cancer (GBC) have a lower 5-year survival rate. Long non-coding RNA urothelial carcinoma associated 1 (UCA1) and miR-613 are involved in the progression of various cancers. This study was to explore the regulatory mechanism between UCA1 and miR-613 in GBC. METHODS: The expression levels of UCA1, miR-613, and SPOCK1 mRNA were detected using qRT-PCR. Cell proliferation, migration, invasion, and apoptosis were determined with MTT, transwell, or flow cytometry assays. The levels of SPOCK1 protein, Bax, cleaved-casp-3, and Bcl-2 were determined by western blot analysis. The relationship between miR-613 and UCA1 or SPOCK1 was verified via dual-luciferase reporter and/or RNA immunoprecipitation (RIP) assays. The role of UCA1 in vivo was confirmed by xenograft assay. RESULTS: UCA1 and SPOCK1 were upregulated while miR-613 was downregulated in GBC tissues and cells. UCA1 silencing blocked tumor growth in vivo , impeded cell proliferation, migration, invasion, and induced cell apoptosis in GBC cells in vitro . Notably, UCA1 acted as a sponge for miR-613, which targeted SPOCK1 in GBC cells. Moreover, miR-613 repressed cell proliferation, migration, invasion, and accelerated cell apoptosis in GBC cells. UCA1 enhancement reversed miR-613 mimic-mediated influence on proliferation, migration, invasion, and apoptosis of GBC cells. UCA1 regulated SPOCK1 expression through miR-613. Furthermore, SPOCK1 elevation overturned UCA1 silencing-mediated the malignant behaviors of GBC cells. CONCLUSION: UCA1 knockdown suppressed GBC progression via downregulating SPOCK1 via sponging miR-613, providing an evidence for UCA1 as a target for GBC treatment.