Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma
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. We established three AdCC cell lines by orthotropic transplantation and in vivo selection: parental, highly me...
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| Veröffentlicht in: | Anticancer research 2018-01, Vol.38 (1), p.187-197 |
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| creator | Ishibashi, Kana Ishii, Kotaro Sugiyama, Goro Sumida, Tomoki Sugiura, Tsuyoshi Kamata, Y U Seki, Katsuhiro Fujinaga, Takahiro Kumamaru, Wataru Kobayashi, Yosuke Hiyake, Naomi Nakano, Hiroyuki Yamada, Tomohiro Mori, Yoshihide |
| description | 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.
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.
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.
NNMT is a potential biomarker of AdCC. |
| doi_str_mv | 10.21873/anticanres.12207 |
| format | Article |
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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.
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.
NNMT is a potential biomarker of AdCC.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>DOI: 10.21873/anticanres.12207</identifier><identifier>PMID: 29277772</identifier><language>eng</language><publisher>Greece: International Institute of Anticancer Research</publisher><subject>Adenoid ; Biomarkers ; Biotechnology ; Deoxyribonucleic acid ; Deregulation ; DNA ; DNA chips ; DNA microarrays ; Gene expression ; Identification methods ; Lymph nodes ; Mesenchyme ; Metastases ; Metastasis ; Methyltransferase ; N-Methyltransferase ; Nicotinamide ; Nicotinamide N-methyltransferase ; Proteins ; Salivary gland ; Salivary glands ; Stem cells ; Transplantation ; Tumorigenesis ; Tumors</subject><ispartof>Anticancer research, 2018-01, Vol.38 (1), p.187-197</ispartof><rights>Copyright© 2018, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.</rights><rights>Copyright International Institute of Anticancer Research Jan 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-a7f68502d5d1040dd31fab1bd84d0d1eed3274ec21f6b301d0d254d8001426ac3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29277772$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ishibashi, Kana</creatorcontrib><creatorcontrib>Ishii, Kotaro</creatorcontrib><creatorcontrib>Sugiyama, Goro</creatorcontrib><creatorcontrib>Sumida, Tomoki</creatorcontrib><creatorcontrib>Sugiura, Tsuyoshi</creatorcontrib><creatorcontrib>Kamata, Y U</creatorcontrib><creatorcontrib>Seki, Katsuhiro</creatorcontrib><creatorcontrib>Fujinaga, Takahiro</creatorcontrib><creatorcontrib>Kumamaru, Wataru</creatorcontrib><creatorcontrib>Kobayashi, Yosuke</creatorcontrib><creatorcontrib>Hiyake, Naomi</creatorcontrib><creatorcontrib>Nakano, Hiroyuki</creatorcontrib><creatorcontrib>Yamada, Tomohiro</creatorcontrib><creatorcontrib>Mori, Yoshihide</creatorcontrib><title>Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>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.
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.
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.
NNMT is a potential biomarker of AdCC.</description><subject>Adenoid</subject><subject>Biomarkers</subject><subject>Biotechnology</subject><subject>Deoxyribonucleic acid</subject><subject>Deregulation</subject><subject>DNA</subject><subject>DNA chips</subject><subject>DNA microarrays</subject><subject>Gene expression</subject><subject>Identification methods</subject><subject>Lymph nodes</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Methyltransferase</subject><subject>N-Methyltransferase</subject><subject>Nicotinamide</subject><subject>Nicotinamide N-methyltransferase</subject><subject>Proteins</subject><subject>Salivary gland</subject><subject>Salivary glands</subject><subject>Stem cells</subject><subject>Transplantation</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpdkUFv1DAQhS0EokvhB3BBlrhwSZmxk9h7rBZoQaXtAc7RbDyhrhJ7sZPDnvrXMdsWpI5GGmnme08jPSHeIpwotEZ_pDD7nkLifIJKgXkmVmjWWJlGw3OxAtVAZQCaI_Eq51uAtl1b_VIcqbUypdRK3H3ixL-WkWYfg4yDvPR9nH2gyTuWl9V3nm_245wo5IETZZYUnDyjnfy2hP4guk5xZh_k6bi7oQrlhpbMWRYl5dI-y79HxyF6Jzf7XF4uTOp9iBO9Fi8GGjO_eZjH4ueXzz8259XF1dnXzelF1dfazhWZobUNKNc4hBqc0zjQFrfO1g4cMjutTM29wqHdasCyVE3tLADWqqVeH4sP9767FH8vnOdu8rnncaTAcckdri002tatKuj7J-htXFIo33UKtW3BNGgKhfdUn2LOiYdul_xEad8hdId0uv_pdId0iubdg_Oyndj9UzzGof8A5CiOVQ</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Ishibashi, Kana</creator><creator>Ishii, Kotaro</creator><creator>Sugiyama, Goro</creator><creator>Sumida, Tomoki</creator><creator>Sugiura, Tsuyoshi</creator><creator>Kamata, Y U</creator><creator>Seki, Katsuhiro</creator><creator>Fujinaga, Takahiro</creator><creator>Kumamaru, Wataru</creator><creator>Kobayashi, Yosuke</creator><creator>Hiyake, Naomi</creator><creator>Nakano, Hiroyuki</creator><creator>Yamada, Tomohiro</creator><creator>Mori, Yoshihide</creator><general>International Institute of Anticancer Research</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20180101</creationdate><title>Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma</title><author>Ishibashi, Kana ; 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The aim of this study was to identify factors mediating AdCC metastasis.
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.
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.
NNMT is a potential biomarker of AdCC.</abstract><cop>Greece</cop><pub>International Institute of Anticancer Research</pub><pmid>29277772</pmid><doi>10.21873/anticanres.12207</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adenoid Biomarkers Biotechnology Deoxyribonucleic acid Deregulation DNA DNA chips DNA microarrays Gene expression Identification methods Lymph nodes Mesenchyme Metastases Metastasis Methyltransferase N-Methyltransferase Nicotinamide Nicotinamide N-methyltransferase Proteins Salivary gland Salivary glands Stem cells Transplantation Tumorigenesis Tumors |
| title | Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma |
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