LncRNA ARAP1-AS1 Promotes Bladder Cancer Development by Regulating the miR-3918/KIF20A Axis

This study is to clarify the effect of the long non-coding RNA ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 1-antisense RNA 1 (ARAP1-AS1)/microRNA (miR)-3918/kinesin family member 20A (KIF20A) on bladder cancer cell function. ARAP1-AS1, miR-3918, and KIF20A expression levels in bladder cancer cells were determined using quantitative reverse transcription-polymerase chain reaction. The effects of ARAP1-AS1, miR-3918, and KIF20A on bladder cell activity, proliferation, apoptosis, and in vivo growth were examined using the cell counting kit-8, colony formation, caspase-3 activity, and xenograft tumor growth assays, respectively, in nude mice. The binding relationships among ARAP1-AS1, miR-3918, and KIF20A were analyzed using luciferase and RNA immunoprecipitation assays. ARAP1-AS1 and KIF20A were overexpressed in bladder cancer, while miR-3918 was underexpressed. The downregulation of ARAP1-AS1 or KIF20A expression significantly inhibited the viability and proliferation of cancer cells and promoted apoptosis, whereas low expression of miR-3918 or high expression of ARAP1-AS1/KIF20A showed the opposite effect. miR-3918 was sponged by ARAP1-AS1, and targeted KIF20A. In addition, miR-3918 expression was inversely correlated with ARAP1-AS1 and KIF20a expression levels in bladder cancer tissues. In addition, the rescue experiment showed that interference with miR-3918 could reverse the effect of low ARAP1-AS1 or KIF20A expression on bladder cancer cell malignancy. ARAP1-AS1 facilitates the malignant behavior of bladder cancer cells via the regulation of KIF20A expression by sponging miR-3918.