Upregulated H19 contributes to bladder cancer cell proliferation by regulating ID2 expression

Long noncoding RNAs have been shown to have important regulatory roles in cancer biology, and long noncoding RNA19 (H19) is essential for human tumor growth. However, little is known about how abnormal expression of H19 contributes to bladder cancer cell proliferation. In this study, we first evaluated the expression of H19 in bladder cancer tissues by real-time PCR, and defined the biological functions. We found that H19 expression levels were remarkably increased in bladder cancer tissues as compared with adjacent normal control tissue, and forced expression of H19 promoted bladder cancer cell proliferation invitro. Inhibitor of DNA binding/differentiation2 (ID2) expression levels were upregulated in bladder cancer tissues and in bladder cancer cells. A significant positive correlation was observed between H19 levels and ID2 levels invivo. We further demonstrated that overexpression of H19 resulted in a significant increase in the expression of ID2, whereas H19 knockdown decreased ID2 expression invitro. Gain-of-function and loss-of-function studies demonstrated that upregulated H19 increased bladder cancer cell proliferation by increasing ID2 expression. In conclusion, upregulated H19 increases bladder cancer growth by regulating ID2 expression, and thus may be helpful in the development of effective treatment strategies for bladder cancer. Structured digital abstract TfR1-Cp and TfR1-Cp bind by comigration in gel electrophoresis (View interaction) HSA and TfR1-Cp bind by comigration in gel electrophoresis (View interaction) SPPL2B and TfR1-NTF colocalize by fluorescence microscopy (View interaction) SPPL2A and TfR1-NTF colocalize by fluorescence microscopy (View interaction) HSA binds to TfR1-Cp by pull down (View interaction) TfR1-Cp and TfR1-Cp bind by comigration in gel electrophoresis (View interaction)