Opposite regulation of epithelial-to-mesenchymal transition and cell invasiveness by periostin between prostate and bladder cancer cells.

We previously showed that periostin expression is downregulated in human bladder cancer tissues and that ectopic expression of periostin suppresses the invasiveness of bladder cancer cells. However, in most other human cancers studied, the expression of periostin promotes cell invasiveness. In the present study, we investigated the regulation of the epithelial-to-mesenchymal transition (EMT) and cell invasiveness by periostin in bladder and prostate cancer cell lines, and found opposite regulation of EMT and cell invasiveness by periostin. Periostin upregulated E-cadherin expression in bladder cancer cells but downregulated it in prostate cancer cells. Periostin suppressed cell invasiveness in bladder cancer cells but promoted it in prostate cancer cells. Snail, a negative regulator of E-cadherin, was upregulated by periostin in prostate cancer cells, while Twist, another negative regulator of E-cadherin, was downregulated in bladder cancer cells. The C-terminal region of periostin was sufficient for these functions in bladder cancer cells but not in prostate cancer cells. Knockdown of endogenous Snail by siRNA suppressed cell invasiveness in prostate cancer cells expressing periostin. Periostin also suppressed Akt phosphorylation in bladder cancer cells but enhanced it in prostate cancer cells. Treatment with Akt inhibitor increased E-cadherin expression and suppressed both Twist expression and cell invasiveness of bladder cancer cells. These results indicate that Akt signaling plays a role in the cell-type-dependent regulation of E-cadherin expression and cell invasiveness by periostin via Snail and Twist.

Citation

Chul Jang Kim, Kanami Sakamoto, Yukihiro Tambe, Hirokazu Inoue. Opposite regulation of epithelial-to-mesenchymal transition and cell invasiveness by periostin between prostate and bladder cancer cells. International journal of oncology. 2011 Jun;38(6):1759-66

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PMID: 21468544

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