English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Altered sialylation, closely associated with tumor progression and metastasis, has been implicated in human thyroid carcinoma. The present study investigated the alteration in expression of ST6GalNAcII involved in invasion and to clarify the possible mechanism of ST6GalNAcII in the metastasis process in human follicular thyroid carcinoma cell lines. Using real-time PCR, western blot and IHC analysis, ST6GalNAcII differed in three follicular thyroid cancer cell lines (FTC133, primary and FTC238, lung metastasis). It also showed differential expression in follicular thyroid carcinoma and tissue specimens. In addition, we analyzed the PI3K/Akt signaling pathway. The altered expression of ST6GalNAcII corresponded to changed invasive phenotype of FTC-238 and FTC-133 cells in vitro and in vivo. Further studies showed that regulating ST6GalNAcII expression markedly modulated the activity of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. Targeting the PI3K/Akt pathway by its specific inhibitor LY294002, or by Akt small interfering RNA (siRNA) resulted in reduced capacity in invasion of FTC-238. In conclusion, taken together, our results imply that ST6GalNAcII activated the invasion in follicular thyroid cancer cells through regulating the activity of PI3K/Akt pathway.

ST6GalNAcII mediates tumor invasion through PI3K/Akt/NF-κB signaling pathway in follicular thyroid carcinoma