PT  - JOURNAL ARTICLE
AU  - ISHIBASHI, KANA
AU  - ISHII, KOTARO
AU  - SUGIYAMA, GORO
AU  - KAMATA, YU
AU  - SUZUKI, AZUSA
AU  - KUMAMARU, WATARU
AU  - OHYAMA, YUKIKO
AU  - NAKANO, HIROYUKI
AU  - KIYOSHIMA, TAMOTSU
AU  - SUMIDA, TOMOKI
AU  - YAMADA, TOMOHIRO
AU  - MORI, YOSHIHIDE
TI  - Regulation of β-Catenin Phosphorylation by PR55β in Adenoid Cystic Carcinoma
DP  - 2018 Jan 01
TA  - Cancer Genomics - Proteomics
PG  - 53--60
VI  - 15
IP  - 1
4099  - http://cgp.iiarjournals.org/content/15/1/53.short
4100  - http://cgp.iiarjournals.org/content/15/1/53.full
SO  - Cancer Genomics Proteomics2018 Jan 01; 15
AB  - 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. β-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 β-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: PR55β was highly expressed in ACCS-M, suggesting its functional importance. In addition, PR55β expression was associated with tumor grade, with ACCS-M exhibiting higher PR55β levels. More importantly, knockdown of PR55β in ACCS-M cells significantly reduced invasiveness and metastatic ability. Furthermore, dephosphorylation and total levels of β-catenin were dependent on PR55β in ACCS-M. Finally, we confirmed a correlation between PR55β staining intensity and histopathological type in human AdCC tissues. Conclusion: Our study provides new insight into the interaction between PR55β and β-catenin and suggests that PR55β may be a target for the clinical treatment of AdCC.