IC-2 Suppresses Proliferation and Induces Apoptosis of Bladder Cancer Cells via the Wnt/β-Catenin Pathway

Background: The Wnt/beta-catenin signaling pathway participates in many important tumorigeneses processes, including bladder cancer. The inhibition of abnormal activation of Wnt pathways might provide a new approach to tumor treatment. In the present study, we investigated the role of IC-2, a novel Wnt pathways small molecular inhibitor, in bladder cancer tumorigenesis. Material/Methods: Bladder cancer cells were treated with various concentrations of IC-2 (0-5 mu M) in vitro. The proliferation ability was measured using colony formation assay and apoptosis was measured using flow cytometry analysis. The protein expression was detected using Western blot analysis. Xenograft in vivo assay was performed to assess tumor growth. Results: IC-2 suppressed the proliferation and aggravated the apoptosis of bladder cancer cells in dose-dependent and time-dependent manners in vitro. Moreover, high concentrations of IC-2 inhibited the Wnt pathway-related protein expression levels, including beta-catenin, Cyclin D1, and TCF4. In vivo, administration of IC-2 in xenograft mice decreased the beta-catenin expression and reduced the tumor volume. Conclusions: Our results validate the tumor-inhibition effect of IC-2 on bladder cancer in vivo and in vitro, providing a novel therapeutic strategy for bladder cancer.