Abstract:
:Integrin-linked kinase (ILK) is a multifunctional serine/threonine kinase. Accumulating evidences suggest that ILK are involved in cell-matrix interactions, cell proliferation, invasion, migration, angiogenesis and Epithelial-mesenchymal transition (EMT). However, the underlying mechanisms remain largely unknown. EMT has been postulated as a prerequisite for metastasis. The reports have demonstrated that EMT was implicated in metastasis of oral squamous cell carcinomas. Therefore, here we further postulate that ILK might participate in EMT of tongue cancer. We showed that ILK siRNA inhibited EMT with low N-cadherin, Vimentin, Snail, Slug and Twist as well as high E-cadherin expression in vivo and in vitro. We found that knockdown of ILK inhibited cell proliferation, migration and invasion as well as changed cell morphology. We also demonstrated that ILK siRNA inhibited phosphorylation of downstream signaling targets Akt and GSK3β as well as reduced expression of MMP2 and MMP9. Furthermore, we found that the tongue tumor with high metastasis capability showed higher ILK, Vimentin, Snail, Slug and Twist as well as lower E-cadherin expression in clinical specimens. Finally, ILK siRNA led to the suppression for tumorigenesis and metastasis in vivo. Our findings suggest that ILK could be a novel diagnostic and therapeutic target for tongue cancer.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Xing Y,Qi J,Deng S,Wang C,Zhang L,Chen Jdoi
10.1016/j.yexcr.2013.05.014subject
Has Abstractpub_date
2013-08-01 00:00:00pages
2058-2072issue
13eissn
0014-4827issn
1090-2422pii
S0014-4827(13)00220-6journal_volume
319pub_type
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