Long non-coding RNA CASC2 targeting miR-18a suppresses glioblastoma cell growth, metastasis and EMTin vitroandin vivo

Long non-coding RNAs (lncRNAs) cancer susceptibility candidate 2 (CASC2) has been characterized as a tumor suppressor in glioma. Although CASC2 may predict the prognosis of glioma patients, the role and mechanism of CASC2 in human glioblastoma remain to be fully illuminated. Expression of CASC2 and miR-18a was detected using RT-qPCR. Cell growth was evaluated by MTT assay, colony formation assay, and flow cytometry; metastasis and epithelial-mesenchymal transition (EMT) were determined with transwell assay and Western blot, respectively. The target binding between CASC2 and miR-18a was predicted onStarbasesoftware, and confirmed by luciferase reporter assay and RNA immunoprecipitation. Xenograft experiment measured tumor growth. As a result, CASC2 was downregulated and miR-18a was upregulated in glioblastoma tumor tissues and cells (T98 and A172). Overexpression of CASC2 promoted apoptosis rate and E-cadherin expression, but suppressed cell viability, colony-forming ability, migration, invasion, and expression of N-cadherin and Vimentin in T98 and A172 cells, accompanied with tumor growth inhibitionin vivo; whereas, silencing of CASC2 exerted the opposite effect on cell growth, metastasis and EMT of T98 and A172 cellsin vitro. However, reintroduction of miR-18a could reverse CASC2 upregulation-mediated suppression on above cell behaviorsin vitro. More importantly, miR-18a was a downstream target for CASC2, and was negatively regulated by CASC2. Collectively, this study demonstrated that CASC2 served as tumor suppressor in glioblastoma by inhibiting cell growth, metastasis and EMT bothin vitroandin vivopartially via CASC2-miR-18a axis.