%0 Journal Article
%T Regulation of ¦Â-Catenin Phosphorylation by PR55¦Â in Adenoid Cystic Carcinoma
%A AZUSA SUZUKI
%A GORO SUGIYAMA
%A HIROYUKI NAKANO
%A KANA ISHIBASHI
%A KOTARO ISHII
%A TAMOTSU KIYOSHIMA
%A TOMOKI SUMIDA1
%A TOMOHIRO YAMADA1
%A YOSHIHIDE MORI
%A WATARU KUMAMARU
%A YU KAMATA
%A YUKIKO OHYAMA
%J Archive of "Cancer Genomics & Proteomics".
%D 2018
%R 10.21873/cgp.20064
%X Background/Aim: Adenoid cystic carcinoma (AdCC) is a rare cancer of the salivary gland with high risk of recurrence and metastasis. Wnt signalling is critical for determining tumor grade in AdCC, as it regulates invasion and migration. ¦Â-catenin dephosphorylation plays an important role in the Wnt pathway, but its underlying molecular mechanism remains unclear. Materials and Methods: Because the regulatory subunits of protein phosphatase 2A (PP2A) drive Wnt signalling via target molecules, including ¦Â-catenin, we used qRT-PCR and immunoblot analysis to investigate the expression of these subunits in an AdCC cell line (ACCS) and a more aggressive subline (ACCS-M). Results: PR55¦Â was highly expressed in ACCS-M, suggesting its functional importance. In addition, PR55¦Â expression was associated with tumor grade, with ACCS-M exhibiting higher PR55¦Â levels. More importantly, knockdown of PR55¦Â in ACCS-M cells significantly reduced invasiveness and metastatic ability. Furthermore, dephosphorylation and total levels of ¦Â-catenin were dependent on PR55¦Â in ACCS-M. Finally, we confirmed a correlation between PR55¦Â staining intensity and histopathological type in human AdCC tissues. Conclusion: Our study provides new insight into the interaction between PR55¦Â and ¦Â-catenin and suggests that PR55¦Â may be a target for the clinical treatment of AdCC
%K PP2A
%K PR55¦Â
%K regulatory subunit
%K ¦Â-catenin
%K adenoid cystic carcinoma
%K salivary gland
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5822182/