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Upregulated H19 contributes to bladder cancer cell proliferation by regulating ID2 expression
Author(s) -
Luo Ming,
Li Zuowei,
Wang Wei,
Zeng Yigang,
Liu Zhihong,
Qiu Jianxin
Publication year - 2013
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12185
Subject(s) - downregulation and upregulation , bladder cancer , gene knockdown , cell growth , cancer research , long non coding rna , cancer , colocalization , cancer cell , carcinogenesis , cell , biology , microbiology and biotechnology , chemistry , cell culture , gene , biochemistry , genetics
Long noncoding RNA s have been shown to have important regulatory roles in cancer biology, and long noncoding RNA 19 (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 in vitro . Inhibitor of DNA binding/differentiation 2 ( ID 2) expression levels were upregulated in bladder cancer tissues and in bladder cancer cells. A significant positive correlation was observed between H19 levels and ID 2 levels in vivo . We further demonstrated that overexpression of H19 resulted in a significant increase in the expression of ID 2, whereas H19 knockdown decreased ID 2 expression in vitro . Gain‐of‐function and loss‐of‐function studies demonstrated that upregulated H19 increased bladder cancer cell proliferation by increasing ID 2 expression. In conclusion, upregulated H19 increases bladder cancer growth by regulating ID 2 expression, and thus may be helpful in the development of effective treatment strategies for bladder cancer. Structured digital abstractTfR1-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 )