RT Journal Article
SR Electronic
T1 Regulation of β-Catenin Phosphorylation by PR55β in Adenoid Cystic Carcinoma
JF Cancer Genomics - Proteomics
JO Cancer Genomics Proteomics
FD International Institute of Anticancer Research
SP 53
OP 60
VO 15
IS 1
A1 ISHIBASHI, KANA
A1 ISHII, KOTARO
A1 SUGIYAMA, GORO
A1 KAMATA, YU
A1 SUZUKI, AZUSA
A1 KUMAMARU, WATARU
A1 OHYAMA, YUKIKO
A1 NAKANO, HIROYUKI
A1 KIYOSHIMA, TAMOTSU
A1 SUMIDA, TOMOKI
A1 YAMADA, TOMOHIRO
A1 MORI, YOSHIHIDE
YR 2018
UL http://cgp.iiarjournals.org/content/15/1/53.abstract
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.