TY - JOUR T1 - Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma JF - Anticancer Research JO - Anticancer Res SP - 187 LP - 197 VL - 38 IS - 1 AU - KANA ISHIBASHI AU - KOTARO ISHII AU - GORO SUGIYAMA AU - TOMOKI SUMIDA AU - TSUYOSHI SUGIURA AU - YU KAMATA AU - KATSUHIRO SEKI AU - TAKAHIRO FUJINAGA AU - WATARU KUMAMARU AU - YOSUKE KOBAYASHI AU - NAOMI HIYAKE AU - HIROYUKI NAKANO AU - TOMOHIRO YAMADA AU - YOSHIHIDE MORI Y1 - 2018/01/01 UR - http://ar.iiarjournals.org/content/38/1/187.abstract N2 - Background/Aim: Adenoid cystic carcinoma (AdCC) is a malignant tumor that occurs in the salivary glands and frequently metastasizes. The aim of this study was to identify factors mediating AdCC metastasis. Materials and Methods: We established three AdCC cell lines by orthotropic transplantation and in vivo selection: parental, highly metastatic (ACCS-M-GFP), and lymph node metastatic (ACCS-LN-GFP) cells. Results: We examined the three cell lines. DNA microarray indicated significantly altered processes in ACCS-LN-GFP cells: particularly, the expression of nicotinamide N-methyltransferase (NNMT) was enhanced the most. NNMT is associated with tumorigenesis and is a potential tumor biomarker. Concomitantly, we found-significant down-regulation of gap junction protein alpha-1. We suggest that ACCS-LN-GFP cells acquire cancer stem cell features involving the up-regulation of NNMT and the loss of gap junction protein alpha-1, leading to epithelial–mesenchymal transition and consequent AdCC metastasis. Conclusion: NNMT is a potential biomarker of AdCC. ER -