PT  - JOURNAL ARTICLE
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
TI  - Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma
DP  - 2018 Jan 01
TA  - Anticancer Research
PG  - 187--197
VI  - 38
IP  - 1
4099  - http://ar.iiarjournals.org/content/38/1/187.short
4100  - http://ar.iiarjournals.org/content/38/1/187.full
SO  - Anticancer Res2018 Jan 01; 38
AB  - 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.