Fad104, a positive regulator of adipocyte differentiation, suppresses invasion and metastasis of melanoma cells by inhibition of STAT3 activity
Metastasis is the main cause of death in patients with cancer, and understanding the mechanisms of metastatic processes is essential for the development of cancer therapy. Although the role of several cell adhesion, migration or proliferation molecules in metastasis is established, a novel target fo...
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description | Metastasis is the main cause of death in patients with cancer, and understanding the mechanisms of metastatic processes is essential for the development of cancer therapy. Although the role of several cell adhesion, migration or proliferation molecules in metastasis is established, a novel target for cancer therapy remains to be discovered. Previously, we reported that fad104 (factor for adipocyte differentiation 104), a regulatory factor of adipogenesis, regulates cell adhesion and migration. In this report, we clarify the role of fad104 in the invasion and metastasis of cancer cells. The expression level of fad104 in highly metastatic melanoma A375SM cells was lower than that in poorly metastatic melanoma A375C6 cells. Reduction of fad104 expression enhanced the migration and invasion of melanoma cells, while over-expression of FAD104 inhibited migration and invasion. In addition, melanoma cells stably expressing FAD104 showed a reduction in formation of lung colonization compared with control cells. FAD104 interacted with STAT3 and down-regulated the phosphorylation level of STAT3 in melanoma cells. These findings together demonstrate that fad104 suppressed the invasion and metastasis of melanoma cells by inhibiting activation of the STAT3 signaling pathway. These findings will aid a comprehensive description of the mechanism that controls the invasion and metastasis of cancer cells. |
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Although the role of several cell adhesion, migration or proliferation molecules in metastasis is established, a novel target for cancer therapy remains to be discovered. Previously, we reported that fad104 (factor for adipocyte differentiation 104), a regulatory factor of adipogenesis, regulates cell adhesion and migration. In this report, we clarify the role of fad104 in the invasion and metastasis of cancer cells. The expression level of fad104 in highly metastatic melanoma A375SM cells was lower than that in poorly metastatic melanoma A375C6 cells. Reduction of fad104 expression enhanced the migration and invasion of melanoma cells, while over-expression of FAD104 inhibited migration and invasion. In addition, melanoma cells stably expressing FAD104 showed a reduction in formation of lung colonization compared with control cells. FAD104 interacted with STAT3 and down-regulated the phosphorylation level of STAT3 in melanoma cells. These findings together demonstrate that fad104 suppressed the invasion and metastasis of melanoma cells by inhibiting activation of the STAT3 signaling pathway. These findings will aid a comprehensive description of the mechanism that controls the invasion and metastasis of cancer cells.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0117197</identifier><identifier>PMID: 25671570</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenoviruses ; Adhesion ; Adipocytes ; Adipocytes - pathology ; Adipogenesis ; Breast cancer ; Cancer ; Cell adhesion ; Cell adhesion & migration ; Cell adhesion molecules ; Cell cycle ; Cell Differentiation ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Colonization ; Development and progression ; Differentiation ; Fibronectins - genetics ; Fibronectins - metabolism ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Humans ; Infections ; Kinases ; Lungs ; Melanoma ; Melanoma - pathology ; Metastases ; Metastasis ; MicroRNAs ; Molecular biology ; Molecular chains ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Overexpression ; Pharmaceutical sciences ; Phosphorylation ; Physiological aspects ; Proteins ; Reduction ; Risk factors ; Signal Transduction ; Skin cancer ; Stat3 protein ; STAT3 Transcription Factor - antagonists & inhibitors ; STAT3 Transcription Factor - metabolism ; Systematic review ; Therapy ; Tumors</subject><ispartof>PloS one, 2015-02, Vol.10 (2), p.e0117197-e0117197</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Katoh et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Katoh et al 2015 Katoh et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-be292fd552eebd87259e2c779b90f5051fd7d9deaa62a8297c62db9e346786c73</citedby><cites>FETCH-LOGICAL-c758t-be292fd552eebd87259e2c779b90f5051fd7d9deaa62a8297c62db9e346786c73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324941/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324941/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25671570$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Yang, Chengfeng</contributor><creatorcontrib>Katoh, Daiki</creatorcontrib><creatorcontrib>Nishizuka, Makoto</creatorcontrib><creatorcontrib>Osada, Shigehiro</creatorcontrib><creatorcontrib>Imagawa, Masayoshi</creatorcontrib><title>Fad104, a positive regulator of adipocyte differentiation, suppresses invasion and metastasis of melanoma cells by inhibition of STAT3 activity</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Metastasis is the main cause of death in patients with cancer, and understanding the mechanisms of metastatic processes is essential for the development of cancer therapy. Although the role of several cell adhesion, migration or proliferation molecules in metastasis is established, a novel target for cancer therapy remains to be discovered. Previously, we reported that fad104 (factor for adipocyte differentiation 104), a regulatory factor of adipogenesis, regulates cell adhesion and migration. In this report, we clarify the role of fad104 in the invasion and metastasis of cancer cells. The expression level of fad104 in highly metastatic melanoma A375SM cells was lower than that in poorly metastatic melanoma A375C6 cells. Reduction of fad104 expression enhanced the migration and invasion of melanoma cells, while over-expression of FAD104 inhibited migration and invasion. In addition, melanoma cells stably expressing FAD104 showed a reduction in formation of lung colonization compared with control cells. FAD104 interacted with STAT3 and down-regulated the phosphorylation level of STAT3 in melanoma cells. These findings together demonstrate that fad104 suppressed the invasion and metastasis of melanoma cells by inhibiting activation of the STAT3 signaling pathway. These findings will aid a comprehensive description of the mechanism that controls the invasion and metastasis of cancer cells.</description><subject>Adenoviruses</subject><subject>Adhesion</subject><subject>Adipocytes</subject><subject>Adipocytes - pathology</subject><subject>Adipogenesis</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Cell cycle</subject><subject>Cell Differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Colonization</subject><subject>Development and progression</subject><subject>Differentiation</subject><subject>Fibronectins - genetics</subject><subject>Fibronectins - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Infections</subject><subject>Kinases</subject><subject>Lungs</subject><subject>Melanoma</subject><subject>Melanoma - pathology</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>Molecular biology</subject><subject>Molecular chains</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis</subject><subject>Overexpression</subject><subject>Pharmaceutical sciences</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Reduction</subject><subject>Risk factors</subject><subject>Signal Transduction</subject><subject>Skin cancer</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - antagonists & inhibitors</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Systematic review</subject><subject>Therapy</subject><subject>Tumors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1FrFDEQxxdRbK1-A9GAIAq9M8lukt0X4ShWDwoFW30N2WT2LmV3sybZ4n0Kv7LZ9lq60gfZwIbJb_6Tmcxk2WuClyQX5NOVG32v2uXgelhiQgSpxJPskFQ5XXCK86cP9gfZixCuMGZ5yfnz7IAyLggT-DD7c6oMwcUxUmhwwUZ7DcjDZmxVdB65BiljB6d3EZCxTQMe-mhVtK4_RmEcBg8hQEC2v1YhGZHqDeogqpCWDZNAB63qXaeQhrYNqN4leGtrO2lM5xeXq8scKZ1C27h7mT1rVBvg1f5_lP04_XJ58m1xdv51fbI6W2jByriogVa0MYxRgNqUgrIKqBaiqivcMMxIY4SpDCjFqSppJTSnpq4gL7gouRb5Ufb2VndoXZD7WgZJOCt4UZUcJ2J9SxinruTgbaf8Tjpl5Y3B-Y1UPlrdgmw0J1xjw4XIC9BlyWpNmroGwXja8aT1eR9trDswOhXRq3YmOj_p7VZu3LUsclpUBUkCH_YC3v0aIUTZ2TAVVPXgxpt7M8oJJVNm7_5BH89uT21USsD2jUtx9SQqVwUtU-NUuEzU8hEqfQY6q1PjNTbZZw4fZw6JifA7btQYglxffP9_9vznnH3_gN2CauM2uHacmijMweIW1N6F4KG5LzLBcpqbu2rIaW7kfm6S25uHD3TvdDco-V87VhT1</recordid><startdate>20150211</startdate><enddate>20150211</enddate><creator>Katoh, Daiki</creator><creator>Nishizuka, Makoto</creator><creator>Osada, Shigehiro</creator><creator>Imagawa, Masayoshi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150211</creationdate><title>Fad104, a positive regulator of adipocyte differentiation, suppresses invasion and metastasis of melanoma cells by inhibition of STAT3 activity</title><author>Katoh, Daiki ; Nishizuka, Makoto ; Osada, Shigehiro ; Imagawa, Masayoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-be292fd552eebd87259e2c779b90f5051fd7d9deaa62a8297c62db9e346786c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adenoviruses</topic><topic>Adhesion</topic><topic>Adipocytes</topic><topic>Adipocytes - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Katoh, Daiki</au><au>Nishizuka, Makoto</au><au>Osada, Shigehiro</au><au>Imagawa, Masayoshi</au><au>Yang, Chengfeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fad104, a positive regulator of adipocyte differentiation, suppresses invasion and metastasis of melanoma cells by inhibition of STAT3 activity</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-02-11</date><risdate>2015</risdate><volume>10</volume><issue>2</issue><spage>e0117197</spage><epage>e0117197</epage><pages>e0117197-e0117197</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Metastasis is the main cause of death in patients with cancer, and understanding the mechanisms of metastatic processes is essential for the development of cancer therapy. Although the role of several cell adhesion, migration or proliferation molecules in metastasis is established, a novel target for cancer therapy remains to be discovered. Previously, we reported that fad104 (factor for adipocyte differentiation 104), a regulatory factor of adipogenesis, regulates cell adhesion and migration. In this report, we clarify the role of fad104 in the invasion and metastasis of cancer cells. The expression level of fad104 in highly metastatic melanoma A375SM cells was lower than that in poorly metastatic melanoma A375C6 cells. Reduction of fad104 expression enhanced the migration and invasion of melanoma cells, while over-expression of FAD104 inhibited migration and invasion. In addition, melanoma cells stably expressing FAD104 showed a reduction in formation of lung colonization compared with control cells. FAD104 interacted with STAT3 and down-regulated the phosphorylation level of STAT3 in melanoma cells. These findings together demonstrate that fad104 suppressed the invasion and metastasis of melanoma cells by inhibiting activation of the STAT3 signaling pathway. These findings will aid a comprehensive description of the mechanism that controls the invasion and metastasis of cancer cells.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25671570</pmid><doi>10.1371/journal.pone.0117197</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adenoviruses Adhesion Adipocytes Adipocytes - pathology Adipogenesis Breast cancer Cancer Cell adhesion Cell adhesion & migration Cell adhesion molecules Cell cycle Cell Differentiation Cell Line, Tumor Cell migration Cell Movement Colonization Development and progression Differentiation Fibronectins - genetics Fibronectins - metabolism Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Humans Infections Kinases Lungs Melanoma Melanoma - pathology Metastases Metastasis MicroRNAs Molecular biology Molecular chains Neoplasm Invasiveness Neoplasm Metastasis Overexpression Pharmaceutical sciences Phosphorylation Physiological aspects Proteins Reduction Risk factors Signal Transduction Skin cancer Stat3 protein STAT3 Transcription Factor - antagonists & inhibitors STAT3 Transcription Factor - metabolism Systematic review Therapy Tumors |
title | Fad104, a positive regulator of adipocyte differentiation, suppresses invasion and metastasis of melanoma cells by inhibition of STAT3 activity |
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