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

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)187-197
Number of pages11
JournalAnticancer research
Volume38
Issue number1
DOIs
Publication statusPublished - Jan 2018

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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