BACKGROUND: Recent studies have demonstrated that Linc00152 is highly expressed in multiple cancer types and its genes show tumor-promoting characteristics. However, the efficacy and biological mechanism of Linc00152 in bladder cancer remains unclear.

MATERIAL AND METHODS: We study investigated the relative expression and promoter methylation of Linc00152 in 126 cases of bladder cancer tissues by qRT-PCR and Bisulfite sequencing PCR. qRT-PCR was used to assess the relative expression of Linc00152 in 4 human bladder cancer cell lines. To explore the biological properties of Linc00152, we performed cell growth and soft-agar colony-formation assays, flow cytometry analyses, wound-healing assay, and Transwell assay. Western blot analysis was used to detect the underlying mechanisms of Linc00152 in bladder cancer.

RESULTS: We found that Linc00152 was highly expressed in 126 cases of bladder carcinoma tissues (p<0.001) and 4 cell lines (p<0.01), and Linc00152 is more commonly expressed in patients with advanced-stage cancer (p=0.021). Knockdown of Linc00152 by using siRNAs in bladder cancer cell lines (T24 and HT-1197) suppressed cell viability and growth by causing cell cycle arrest and apoptosis (p<0.001), as well as inhibiting cell migration and invasion (p<0.001). In addition, the quantitative RT-PCR and Western blot results suggest that knockdown of Linc00152 reduced Wnt/β-Catenin signaling (p<0.001).

CONCLUSIONS: This research shows that Linc00152 is highly expressed in patients with bladder cancer and the possible carcinogenic effect of Linc00152 in bladder cancer occurs through activating the Wnt/β-Catenin signaling pathway, and could be a new biomarker for diagnosis and prevention of this cancer.

Keywords: Cell Growth Processes, Genes, Tumor Suppressor, Cell Cycle Checkpoints