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

doi:10.21873/anticanres.12207

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

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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 language	English
Pages (from-to)	187-197
Number of pages	11
Journal	Anticancer research
Volume	38
Issue number	1
DOIs	https://doi.org/10.21873/anticanres.12207
Publication status	Published - Jan 2018

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.21873/anticanres.12207

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Ishibashi, K., Ishii, K., Sugiyama, G., Sumida, T., Sugiura, T., Kamata, Y., Seki, K., Fujinaga, T., Kumamaru, W., Kobayashi, Y., Hiyake, N., Nakano, H., Yamada, T., & Mori, Y. (2018). Deregulation of nicotinamide N-methyltransferase and gap junction protein alpha-1 causes metastasis in adenoid cystic carcinoma. Anticancer research, 38(1), 187-197. https://doi.org/10.21873/anticanres.12207

Ishibashi, K, Ishii, K, Sugiyama, G, Sumida, T, Sugiura, T, Kamata, Y, Seki, K, Fujinaga, T , Kumamaru, W, Kobayashi, Y, Hiyake, N, Nakano, H, Yamada, T & Mori, Y 2018, 'Deregulation of nicotinamide N-methyltransferase and gap junction protein alpha-1 causes metastasis in adenoid cystic carcinoma', Anticancer research, vol. 38, no. 1, pp. 187-197. https://doi.org/10.21873/anticanres.12207

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

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.",

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

note = "Funding Information: This work was supported by JSPS KAKENHI Grant Number GAG5K20540 and 15K11257. The Authors gratefully acknowledge this financial support. The Authors would also like to thank Editage for English language editing. Copyright: Copyright 2018 Elsevier B.V., All rights reserved.",

year = "2018",

month = jan,

doi = "10.21873/anticanres.12207",

language = "English",

volume = "38",

pages = "187--197",

journal = "Anticancer Research",

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T1 - Deregulation of nicotinamide N-methyltransferase and gap junction protein alpha-1 causes metastasis in adenoid cystic carcinoma

AU - Ishibashi, Kana

AU - Ishii, Kotaro

AU - Sugiyama, Goro

AU - Sumida, Tomoki

AU - Sugiura, Tsuyoshi

AU - Kamata, Yu

AU - Seki, Katsuhiro

AU - Fujinaga, Takahiro

AU - Kumamaru, Wataru

AU - Kobayashi, Yosuke

AU - Hiyake, Naomi

AU - Nakano, Hiroyuki

AU - Yamada, Tomohiro

AU - Mori, Yoshihide

N1 - Funding Information: This work was supported by JSPS KAKENHI Grant Number GAG5K20540 and 15K11257. The Authors gratefully acknowledge this financial support. The Authors would also like to thank Editage for English language editing. Copyright: Copyright 2018 Elsevier B.V., All rights reserved.

PY - 2018/1

Y1 - 2018/1

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.

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.

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

Abstract

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