Background: Growing evidence has indicated that the (), frequently deregulated in almost all tumor types tested, acted as a pivotal contributor to both cancer initiation and progression. However, the role of in human papillary thyroid carcinoma (PTC) remains controversial. The aim of the study was to investigate the expression and potential function of in human PTC.
Patients And Methods: The level was determined by quantitative real-time (RT)-PCR analyses in 58 PTC tissue samples and their paired paracancerous tissue samples. RNA interference, RT-PCR analysis, and Western blot assay were used to determine the impact of on epithelial-mesenchymal transition (EMT) markers in human PTC cells. The migratory and invasive capacities of PTC cells were determined by wound-healing and transwell migration and invasion assays.
Results: expression was 2.417-fold higher in PTC tissues than their paired paracancerous tissue (95% CI: 1.898-2.935, <0.0001). Higher level of was correlated to elevated expression of , , , and . Inhibition of resulted in upregulation of and downregulation of both at mRNA and protein levels. Conversely, enforced expression of the exogenous led to and protein downregulation and relative upregulation of . Moreover, wound-healing and transwell migration and invasion assays showed that could promote the migratory and invasive abilities of PTC cells.
Conclusion: The level of was significantly higher in PTC tissues than paired paracancerous tissue or normal tissues. Overexpression of was correlated with higher tumor burden of PTC. It also contributes to EMT process, as well as promotes migration and invasion of PTC cells.
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| http://dx.doi.org/10.2147/CMAR.S195906 | DOI Listing |
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