Abstract
Cadherin switch is specific of epithelial-mesenchymal transition (EMT) and is closely related to tumor cell invasion. However, the molecular mechanism that promotes the phenotypic changes remains unclear and elusive. We found that integrin-linked kinase (ILK) is a key factor involved in cadherin switch. The expression and activity of ILK are elevated in a variety of cancers but its mechanisms are not exactly understood. In this report, we studied the role and mechanism of ILK in EMT of human bladder cancer. We showed that silencing of ILK expression by small interfering RNA (siRNA) significantly abolished the nuclear translocation or the presence of markers associated with EMT like Snail, Twist, Zeb, and beta-catenin. ILK knockdown by siRNA suppressed N-cadherin expression and increased re-expression of E-cadherin in bladder cancer cells. We suggest that ILK is a major signaling factor involved in EMT. It is essential to understand the molecular mechanism of EMT in aim to possibly use it in search for new therapeutic targets.Electronic supplementary materialThe online version of this article (doi:10.1007/s13277-016-5354-x) contains supplementary material, which is available to authorized users.
Highlights
Bladder cancer is the ninth most frequently diagnosed cancer and the 12th leading cause of deaths worldwide
Loss of E-cadherin expression and induction of N-cadherin expression are a hallmark of the Epihtelial-mesenchymal transition (EMT) process, which is needed for epithelial cells to adopt mesenchymal characteristic, a process known as the cadherin switch [2]
glycogen synthase kinase -3β (GSK-3β) possesses a tyrosine phosphorylation site (Tyr 216) that upon phoshporylation increases its activity [12]. small interfering RNA (siRNA) silencing of integrinlinked kinase (ILK) was sufficient for the activation of GSK-3β because the phosphorylation of GSK3β on Tyr 216 was significantly higher, while phosphorylation on Ser 9 was markedly lower compared with control nonsilencing RNA-treated bladder cells (Fig. 1)
Summary
Bladder cancer is the ninth most frequently diagnosed cancer and the 12th leading cause of deaths worldwide. It is the Electronic supplementary material The online version of this article (doi:10.1007/s13277-016-5354-x) contains supplementary material, which is available to authorized users. Epihtelial-mesenchymal transition (EMT) is a process by which epithelial cells lose their epithelial properties and obtain a mesenchymal phenotype. Tumor cells undergo epithelial to mesenchymal transition which transforms them from a quiescent cancer cells to a malignant phenotype. Loss of E-cadherin expression and induction of N-cadherin expression are a hallmark of the EMT process, which is needed for epithelial cells to adopt mesenchymal characteristic, a process known as the cadherin switch [2]. Supression of E-cadherin expression by transcriptional factors, including Snail, Twist, and Zeb, is engaged in various malignancies
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