NRSF/REST regulates the mTOR signaling pathway in oral cancer cells
The neuron-restrictive silencer factor/repressor element 1-silencing transcription factor (NRSF/REST) was originally discovered as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it was recently reported to be abundantly expressed in several types of aggressive cancer c...
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| Veröffentlicht in: | Oncology reports 2015-03, Vol.33 (3), p.1459-1464 |
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| creator | CHO, EUGENE MOON, SUNG-MIN PARK, BO RAM KIM, DO KYUNG LEE, BYUNG-KWON KIM, CHUN SUNG |
| description | The neuron-restrictive silencer factor/repressor element 1-silencing transcription factor (NRSF/REST) was originally discovered as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it was recently reported to be abundantly expressed in several types of aggressive cancer cells, as well as in mature neurons. In the present study, the role of NRSF/REST in the human oral squamous cell carcinoma (SCC) KB cell line was evaluated. NRSF/REST was expressed at a higher level in KB cells when compared with that in normal human oral keratinocytes (NHOKs). Knockdown of NRSF/REST by siRNA reduced cell viability only in KB cells in a time-dependent manner, and this effect was due to the activation of apoptosis components and DNA fragmentation. In addition, knockdown of NRSF/REST disrupted the mTOR signaling pathway which is a key survival factor in many types of cancer cells. For example, the phosphorylation of elF4G, elF4E and 4E-BP1 was significantly reduced in the KB cells upon NRSF/REST knockdown. These results imply that NRSF/REST plays an important role in the survival of oral cancer cells by regulating the mTOR signaling pathway. |
| doi_str_mv | 10.3892/or.2014.3675 |
| format | Article |
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However, it was recently reported to be abundantly expressed in several types of aggressive cancer cells, as well as in mature neurons. In the present study, the role of NRSF/REST in the human oral squamous cell carcinoma (SCC) KB cell line was evaluated. NRSF/REST was expressed at a higher level in KB cells when compared with that in normal human oral keratinocytes (NHOKs). Knockdown of NRSF/REST by siRNA reduced cell viability only in KB cells in a time-dependent manner, and this effect was due to the activation of apoptosis components and DNA fragmentation. In addition, knockdown of NRSF/REST disrupted the mTOR signaling pathway which is a key survival factor in many types of cancer cells. For example, the phosphorylation of elF4G, elF4E and 4E-BP1 was significantly reduced in the KB cells upon NRSF/REST knockdown. These results imply that NRSF/REST plays an important role in the survival of oral cancer cells by regulating the mTOR signaling pathway.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2014.3675</identifier><identifier>PMID: 25524378</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adaptor Proteins, Signal Transducing - metabolism ; Apoptosis ; Apoptosis - genetics ; Cancer ; Cancer cells ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; Cell Survival - genetics ; Colorectal cancer ; Comparative analysis ; Deoxyribonucleic acid ; DNA ; DNA Fragmentation ; DNA methylation ; DNA-Binding Proteins - metabolism ; human oral squamous cell carcinoma ; Humans ; Laboratories ; Mouth cancer ; Mouth Neoplasms - genetics ; Mouth Neoplasms - pathology ; mTOR signaling ; Neuroblastoma ; NRSF/REST ; Oncology, Experimental ; Oral cancer ; Phosphoproteins - metabolism ; Phosphorylation ; Physiological aspects ; Proteins ; Repressor Proteins - biosynthesis ; Repressor Proteins - genetics ; RNA Interference ; RNA, Small Interfering ; Signal Transduction - genetics ; Squamous cell carcinoma ; TOR Serine-Threonine Kinases - metabolism ; Transcription factors ; Transcription Factors - metabolism ; Tumorigenesis</subject><ispartof>Oncology reports, 2015-03, Vol.33 (3), p.1459-1464</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-6a268e55c384c5a0b9c78357bee7b3bdf7f80162867bf7631fc9d474ecf816de3</citedby><cites>FETCH-LOGICAL-c447t-6a268e55c384c5a0b9c78357bee7b3bdf7f80162867bf7631fc9d474ecf816de3</cites></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/25524378$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHO, EUGENE</creatorcontrib><creatorcontrib>MOON, SUNG-MIN</creatorcontrib><creatorcontrib>PARK, BO RAM</creatorcontrib><creatorcontrib>KIM, DO KYUNG</creatorcontrib><creatorcontrib>LEE, BYUNG-KWON</creatorcontrib><creatorcontrib>KIM, CHUN SUNG</creatorcontrib><title>NRSF/REST regulates the mTOR signaling pathway in oral cancer cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>The neuron-restrictive silencer factor/repressor element 1-silencing transcription factor (NRSF/REST) was originally discovered as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it was recently reported to be abundantly expressed in several types of aggressive cancer cells, as well as in mature neurons. In the present study, the role of NRSF/REST in the human oral squamous cell carcinoma (SCC) KB cell line was evaluated. NRSF/REST was expressed at a higher level in KB cells when compared with that in normal human oral keratinocytes (NHOKs). Knockdown of NRSF/REST by siRNA reduced cell viability only in KB cells in a time-dependent manner, and this effect was due to the activation of apoptosis components and DNA fragmentation. In addition, knockdown of NRSF/REST disrupted the mTOR signaling pathway which is a key survival factor in many types of cancer cells. For example, the phosphorylation of elF4G, elF4E and 4E-BP1 was significantly reduced in the KB cells upon NRSF/REST knockdown. These results imply that NRSF/REST plays an important role in the survival of oral cancer cells by regulating the mTOR signaling pathway.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - genetics</subject><subject>Colorectal cancer</subject><subject>Comparative analysis</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Fragmentation</subject><subject>DNA methylation</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>human oral squamous cell carcinoma</subject><subject>Humans</subject><subject>Laboratories</subject><subject>Mouth cancer</subject><subject>Mouth Neoplasms - genetics</subject><subject>Mouth Neoplasms - pathology</subject><subject>mTOR signaling</subject><subject>Neuroblastoma</subject><subject>NRSF/REST</subject><subject>Oncology, Experimental</subject><subject>Oral cancer</subject><subject>Phosphoproteins - metabolism</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Repressor Proteins - biosynthesis</subject><subject>Repressor Proteins - genetics</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Signal Transduction - genetics</subject><subject>Squamous cell carcinoma</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Transcription factors</subject><subject>Transcription Factors - metabolism</subject><subject>Tumorigenesis</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpd0clr3DAUBnARGpqlveVcBIWSQzzRvhzDkA1CApMp9CZkWZ5x0FhTyabkv49M0mwn6fDjvffxAXCE0YwqTU5jmhGE2YwKyXfAPpYaV4RR_KX8EcEVpfzPHjjI-QEhIpHQX8Ee4bwQqfbB_HZxf3G6OL9fwuRXY7CDz3BYe7hZ3i1g7la9DV2_gls7rP_ZR9j1MCYboLO98wk6H0L-BnZbG7L__vIegt8X58v5VXVzd3k9P7upHGNyqIQlQnnOHVXMcYtq7aSiXNbey5rWTStbhbAgSsi6lYLi1umGSeZdq7BoPD0Ex89ztyn-HX0ezKbL0wW293HMBouSivESs9Cfn-hDHFPJUpSmREgplX5TKxu86fo2Dsm6aag5Y0hqxJFGRf16p9behmGdYxiHLvb5Izx5hi7FnJNvzTZ1G5seDUZm6srEZKauzNRV4T9ebhzrjW9e8f9y3hbnre2bron51cRUeq0QrTDjmj4BbdSXXw</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>CHO, EUGENE</creator><creator>MOON, SUNG-MIN</creator><creator>PARK, BO RAM</creator><creator>KIM, DO KYUNG</creator><creator>LEE, BYUNG-KWON</creator><creator>KIM, CHUN SUNG</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150301</creationdate><title>NRSF/REST regulates the mTOR signaling pathway in oral cancer cells</title><author>CHO, EUGENE ; MOON, SUNG-MIN ; PARK, BO RAM ; KIM, DO KYUNG ; LEE, BYUNG-KWON ; KIM, CHUN SUNG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-6a268e55c384c5a0b9c78357bee7b3bdf7f80162867bf7631fc9d474ecf816de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - genetics</topic><topic>Colorectal cancer</topic><topic>Comparative analysis</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Fragmentation</topic><topic>DNA methylation</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>human oral squamous cell carcinoma</topic><topic>Humans</topic><topic>Laboratories</topic><topic>Mouth cancer</topic><topic>Mouth Neoplasms - genetics</topic><topic>Mouth Neoplasms - pathology</topic><topic>mTOR signaling</topic><topic>Neuroblastoma</topic><topic>NRSF/REST</topic><topic>Oncology, Experimental</topic><topic>Oral cancer</topic><topic>Phosphoproteins - metabolism</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Repressor Proteins - biosynthesis</topic><topic>Repressor Proteins - genetics</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Signal Transduction - genetics</topic><topic>Squamous cell carcinoma</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Transcription factors</topic><topic>Transcription Factors - metabolism</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHO, EUGENE</creatorcontrib><creatorcontrib>MOON, SUNG-MIN</creatorcontrib><creatorcontrib>PARK, BO RAM</creatorcontrib><creatorcontrib>KIM, DO KYUNG</creatorcontrib><creatorcontrib>LEE, BYUNG-KWON</creatorcontrib><creatorcontrib>KIM, CHUN SUNG</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHO, EUGENE</au><au>MOON, SUNG-MIN</au><au>PARK, BO RAM</au><au>KIM, DO KYUNG</au><au>LEE, BYUNG-KWON</au><au>KIM, CHUN SUNG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NRSF/REST regulates the mTOR signaling pathway in oral cancer cells</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>33</volume><issue>3</issue><spage>1459</spage><epage>1464</epage><pages>1459-1464</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>The neuron-restrictive silencer factor/repressor element 1-silencing transcription factor (NRSF/REST) was originally discovered as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it was recently reported to be abundantly expressed in several types of aggressive cancer cells, as well as in mature neurons. In the present study, the role of NRSF/REST in the human oral squamous cell carcinoma (SCC) KB cell line was evaluated. NRSF/REST was expressed at a higher level in KB cells when compared with that in normal human oral keratinocytes (NHOKs). Knockdown of NRSF/REST by siRNA reduced cell viability only in KB cells in a time-dependent manner, and this effect was due to the activation of apoptosis components and DNA fragmentation. In addition, knockdown of NRSF/REST disrupted the mTOR signaling pathway which is a key survival factor in many types of cancer cells. For example, the phosphorylation of elF4G, elF4E and 4E-BP1 was significantly reduced in the KB cells upon NRSF/REST knockdown. These results imply that NRSF/REST plays an important role in the survival of oral cancer cells by regulating the mTOR signaling pathway.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25524378</pmid><doi>10.3892/or.2014.3675</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Adaptor Proteins, Signal Transducing - metabolism Apoptosis Apoptosis - genetics Cancer Cancer cells Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell Line, Tumor Cell Survival - genetics Colorectal cancer Comparative analysis Deoxyribonucleic acid DNA DNA Fragmentation DNA methylation DNA-Binding Proteins - metabolism human oral squamous cell carcinoma Humans Laboratories Mouth cancer Mouth Neoplasms - genetics Mouth Neoplasms - pathology mTOR signaling Neuroblastoma NRSF/REST Oncology, Experimental Oral cancer Phosphoproteins - metabolism Phosphorylation Physiological aspects Proteins Repressor Proteins - biosynthesis Repressor Proteins - genetics RNA Interference RNA, Small Interfering Signal Transduction - genetics Squamous cell carcinoma TOR Serine-Threonine Kinases - metabolism Transcription factors Transcription Factors - metabolism Tumorigenesis |
| title | NRSF/REST regulates the mTOR signaling pathway in oral cancer cells |
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