Deregulation of nicotinamide N-methyltransferase and gap junction protein alpha-1 causes metastasis in adenoid cystic carcinoma

Kana Ishibashi, Kotaro Ishii, Goro Sugiyama, Tomoki Sumida, Tsuyoshi Sugiura, Yu Kamata, Katsuhiro Seki, Takahiro Fujinaga, Wataru Kumamaru, Yosuke Kobayashi, Naomi Hiyake, Hiroyuki Nakano, Tomohiro Yamada, Yoshihide Mori

研究成果: Contribution to journalArticle査読

2 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)187-197
ページ数11
ジャーナルAnticancer research
38
1
DOI
出版ステータス出版済み - 1 2018

All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 癌研究

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