TNF-α Induces URG-4/URGCP Gene Expression in Hepatoma Cells through Starvation Dependent Manner
URG-4/URGCP is a gene that may be associated with the onset of tumorigenesis and cell cycle regulation. In the literature, there is no study about inflammatory cytokine-mediated URG-4/URGCP regulation. In this study, the effect of TNF-α cytokine was investigated on URG-4/URGCP expression in serum-st...
Gespeichert in:
| Veröffentlicht in: | Biochemical genetics 2021-02, Vol.59 (1), p.300-314 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 314 |
|---|---|
| container_issue | 1 |
| container_start_page | 300 |
| container_title | Biochemical genetics |
| container_volume | 59 |
| creator | Tokay, Esra Sagkan, Rahsan Ilikci Kockar, Feray |
| description | URG-4/URGCP is a gene that may be associated with the onset of tumorigenesis and cell cycle regulation. In the literature, there is no study about inflammatory cytokine-mediated URG-4/URGCP regulation. In this study, the effect of TNF-α cytokine was investigated on URG-4/URGCP expression in serum-starved and serum-cultured hepatoma cells. The effect of TNF-α on hepatoma cells was shown using MTT and Annexin-V/PI staining with flow cytometer analyses. As a result, TNF-α leads to the cytotoxicity of hepatoma cells in serum-starved condition whereas no decrease was detected from serum-cultured condition. TNF-α-mediated URG-4/URGCP expression was determined at mRNA and protein level with qRT-PCR analyses and Western blotting method. URG-4URGCP mRNA expression was upregulated in both serum-starved and serum-cultured hepatoma cells. The transfection studies were carried out with URG-4/URGCP promoter constructs for determining the transcriptional activity. TNF-α caused to the upregulation of the activities of URG/URGCP promoter constructs. The basal activities of the URG-4/URGCP promoter conditions are differential according to serum conditions. In addition, some pathway inhibitors were added into hepatoma cells for blocking specific pathways to find out TNF-α-mediated URG-4/URGCP upregulation at mRNA and protein level. TNF-α used JNK and PI3K pathways for regulating URG-4/URGCP gene at serum-starved Hep3B cells. In serum-cultured condition, wortmannin (PI3K inhibitor), MEK-1 (MAPK inhibitor), and SP600125 (JNK inhibitor) did not inhibit the activation response of TNF-α on URGCP. |
| doi_str_mv | 10.1007/s10528-020-09972-z |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2483427753</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2483427753</sourcerecordid><originalsourceid>FETCH-LOGICAL-c342t-87fbdc8e246b010122c7018de3ff0e5994b64401fda1cd496918c203c6ed13b13</originalsourceid><addsrcrecordid>eNp9kEtOwzAQhi0EglK4AAtkibXp-NEkXqJSChIv8VhbTjKBotYJdoKA03AFrsABOBOG8tixGWvkb_5f-gjZ4rDLAdJB4DAUGQMBDLROBXteIj0-TCVTWqTLpAcACRNaZGtkPYS7uGpQapWsSQlSZYL3iL06PWDvr_TIlV2BgV5fTJgaxDk6pxN0SMePjccQprWjU_f2coiNbeu5pSOczQJtb33d3dzSy9b6B9t-UvvYoCvRtfTEOod-g6xUdhZw8_vtk-uD8dXokB2fTY5Ge8eskEq0LEurvCwyFCrJgQMXokiBZyXKqgIcaq3yRCngVWl5USqdaJ4VAmSRYMllzmWf7CxyG1_fdxhac1d33sVKI1QWO9J0KCMlFlTh6xA8Vqbx07n1T4aD-bRqFlZNtGq-rJrneLT9Hd3lcyx_T340RkAugBC_3A36v-5_Yj8A7n-C2Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2483427753</pqid></control><display><type>article</type><title>TNF-α Induces URG-4/URGCP Gene Expression in Hepatoma Cells through Starvation Dependent Manner</title><source>SpringerLink Journals - AutoHoldings</source><creator>Tokay, Esra ; Sagkan, Rahsan Ilikci ; Kockar, Feray</creator><creatorcontrib>Tokay, Esra ; Sagkan, Rahsan Ilikci ; Kockar, Feray</creatorcontrib><description>URG-4/URGCP is a gene that may be associated with the onset of tumorigenesis and cell cycle regulation. In the literature, there is no study about inflammatory cytokine-mediated URG-4/URGCP regulation. In this study, the effect of TNF-α cytokine was investigated on URG-4/URGCP expression in serum-starved and serum-cultured hepatoma cells. The effect of TNF-α on hepatoma cells was shown using MTT and Annexin-V/PI staining with flow cytometer analyses. As a result, TNF-α leads to the cytotoxicity of hepatoma cells in serum-starved condition whereas no decrease was detected from serum-cultured condition. TNF-α-mediated URG-4/URGCP expression was determined at mRNA and protein level with qRT-PCR analyses and Western blotting method. URG-4URGCP mRNA expression was upregulated in both serum-starved and serum-cultured hepatoma cells. The transfection studies were carried out with URG-4/URGCP promoter constructs for determining the transcriptional activity. TNF-α caused to the upregulation of the activities of URG/URGCP promoter constructs. The basal activities of the URG-4/URGCP promoter conditions are differential according to serum conditions. In addition, some pathway inhibitors were added into hepatoma cells for blocking specific pathways to find out TNF-α-mediated URG-4/URGCP upregulation at mRNA and protein level. TNF-α used JNK and PI3K pathways for regulating URG-4/URGCP gene at serum-starved Hep3B cells. In serum-cultured condition, wortmannin (PI3K inhibitor), MEK-1 (MAPK inhibitor), and SP600125 (JNK inhibitor) did not inhibit the activation response of TNF-α on URGCP.</description><identifier>ISSN: 0006-2928</identifier><identifier>EISSN: 1573-4927</identifier><identifier>DOI: 10.1007/s10528-020-09972-z</identifier><identifier>PMID: 33034821</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>1-Phosphatidylinositol 3-kinase ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell cycle ; Cytokines ; Cytotoxicity ; Gene expression ; Hepatoma ; Human Genetics ; Inflammation ; Inhibitors ; Liver cancer ; MAP kinase ; Medical Microbiology ; Original Article ; Proteins ; Toxicity ; Transcription ; Transfection ; Tumor necrosis factor-α ; Tumorigenesis ; Western blotting ; Wortmannin ; Zoology</subject><ispartof>Biochemical genetics, 2021-02, Vol.59 (1), p.300-314</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-87fbdc8e246b010122c7018de3ff0e5994b64401fda1cd496918c203c6ed13b13</citedby><cites>FETCH-LOGICAL-c342t-87fbdc8e246b010122c7018de3ff0e5994b64401fda1cd496918c203c6ed13b13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10528-020-09972-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10528-020-09972-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33034821$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tokay, Esra</creatorcontrib><creatorcontrib>Sagkan, Rahsan Ilikci</creatorcontrib><creatorcontrib>Kockar, Feray</creatorcontrib><title>TNF-α Induces URG-4/URGCP Gene Expression in Hepatoma Cells through Starvation Dependent Manner</title><title>Biochemical genetics</title><addtitle>Biochem Genet</addtitle><addtitle>Biochem Genet</addtitle><description>URG-4/URGCP is a gene that may be associated with the onset of tumorigenesis and cell cycle regulation. In the literature, there is no study about inflammatory cytokine-mediated URG-4/URGCP regulation. In this study, the effect of TNF-α cytokine was investigated on URG-4/URGCP expression in serum-starved and serum-cultured hepatoma cells. The effect of TNF-α on hepatoma cells was shown using MTT and Annexin-V/PI staining with flow cytometer analyses. As a result, TNF-α leads to the cytotoxicity of hepatoma cells in serum-starved condition whereas no decrease was detected from serum-cultured condition. TNF-α-mediated URG-4/URGCP expression was determined at mRNA and protein level with qRT-PCR analyses and Western blotting method. URG-4URGCP mRNA expression was upregulated in both serum-starved and serum-cultured hepatoma cells. The transfection studies were carried out with URG-4/URGCP promoter constructs for determining the transcriptional activity. TNF-α caused to the upregulation of the activities of URG/URGCP promoter constructs. The basal activities of the URG-4/URGCP promoter conditions are differential according to serum conditions. In addition, some pathway inhibitors were added into hepatoma cells for blocking specific pathways to find out TNF-α-mediated URG-4/URGCP upregulation at mRNA and protein level. TNF-α used JNK and PI3K pathways for regulating URG-4/URGCP gene at serum-starved Hep3B cells. In serum-cultured condition, wortmannin (PI3K inhibitor), MEK-1 (MAPK inhibitor), and SP600125 (JNK inhibitor) did not inhibit the activation response of TNF-α on URGCP.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell cycle</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Gene expression</subject><subject>Hepatoma</subject><subject>Human Genetics</subject><subject>Inflammation</subject><subject>Inhibitors</subject><subject>Liver cancer</subject><subject>MAP kinase</subject><subject>Medical Microbiology</subject><subject>Original Article</subject><subject>Proteins</subject><subject>Toxicity</subject><subject>Transcription</subject><subject>Transfection</subject><subject>Tumor necrosis factor-α</subject><subject>Tumorigenesis</subject><subject>Western blotting</subject><subject>Wortmannin</subject><subject>Zoology</subject><issn>0006-2928</issn><issn>1573-4927</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kEtOwzAQhi0EglK4AAtkibXp-NEkXqJSChIv8VhbTjKBotYJdoKA03AFrsABOBOG8tixGWvkb_5f-gjZ4rDLAdJB4DAUGQMBDLROBXteIj0-TCVTWqTLpAcACRNaZGtkPYS7uGpQapWsSQlSZYL3iL06PWDvr_TIlV2BgV5fTJgaxDk6pxN0SMePjccQprWjU_f2coiNbeu5pSOczQJtb33d3dzSy9b6B9t-UvvYoCvRtfTEOod-g6xUdhZw8_vtk-uD8dXokB2fTY5Ge8eskEq0LEurvCwyFCrJgQMXokiBZyXKqgIcaq3yRCngVWl5USqdaJ4VAmSRYMllzmWf7CxyG1_fdxhac1d33sVKI1QWO9J0KCMlFlTh6xA8Vqbx07n1T4aD-bRqFlZNtGq-rJrneLT9Hd3lcyx_T340RkAugBC_3A36v-5_Yj8A7n-C2Q</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Tokay, Esra</creator><creator>Sagkan, Rahsan Ilikci</creator><creator>Kockar, Feray</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7SS</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope></search><sort><creationdate>20210201</creationdate><title>TNF-α Induces URG-4/URGCP Gene Expression in Hepatoma Cells through Starvation Dependent Manner</title><author>Tokay, Esra ; Sagkan, Rahsan Ilikci ; Kockar, Feray</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-87fbdc8e246b010122c7018de3ff0e5994b64401fda1cd496918c203c6ed13b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell cycle</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>Gene expression</topic><topic>Hepatoma</topic><topic>Human Genetics</topic><topic>Inflammation</topic><topic>Inhibitors</topic><topic>Liver cancer</topic><topic>MAP kinase</topic><topic>Medical Microbiology</topic><topic>Original Article</topic><topic>Proteins</topic><topic>Toxicity</topic><topic>Transcription</topic><topic>Transfection</topic><topic>Tumor necrosis factor-α</topic><topic>Tumorigenesis</topic><topic>Western blotting</topic><topic>Wortmannin</topic><topic>Zoology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tokay, Esra</creatorcontrib><creatorcontrib>Sagkan, Rahsan Ilikci</creatorcontrib><creatorcontrib>Kockar, Feray</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><jtitle>Biochemical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tokay, Esra</au><au>Sagkan, Rahsan Ilikci</au><au>Kockar, Feray</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TNF-α Induces URG-4/URGCP Gene Expression in Hepatoma Cells through Starvation Dependent Manner</atitle><jtitle>Biochemical genetics</jtitle><stitle>Biochem Genet</stitle><addtitle>Biochem Genet</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>59</volume><issue>1</issue><spage>300</spage><epage>314</epage><pages>300-314</pages><issn>0006-2928</issn><eissn>1573-4927</eissn><abstract>URG-4/URGCP is a gene that may be associated with the onset of tumorigenesis and cell cycle regulation. In the literature, there is no study about inflammatory cytokine-mediated URG-4/URGCP regulation. In this study, the effect of TNF-α cytokine was investigated on URG-4/URGCP expression in serum-starved and serum-cultured hepatoma cells. The effect of TNF-α on hepatoma cells was shown using MTT and Annexin-V/PI staining with flow cytometer analyses. As a result, TNF-α leads to the cytotoxicity of hepatoma cells in serum-starved condition whereas no decrease was detected from serum-cultured condition. TNF-α-mediated URG-4/URGCP expression was determined at mRNA and protein level with qRT-PCR analyses and Western blotting method. URG-4URGCP mRNA expression was upregulated in both serum-starved and serum-cultured hepatoma cells. The transfection studies were carried out with URG-4/URGCP promoter constructs for determining the transcriptional activity. TNF-α caused to the upregulation of the activities of URG/URGCP promoter constructs. The basal activities of the URG-4/URGCP promoter conditions are differential according to serum conditions. In addition, some pathway inhibitors were added into hepatoma cells for blocking specific pathways to find out TNF-α-mediated URG-4/URGCP upregulation at mRNA and protein level. TNF-α used JNK and PI3K pathways for regulating URG-4/URGCP gene at serum-starved Hep3B cells. In serum-cultured condition, wortmannin (PI3K inhibitor), MEK-1 (MAPK inhibitor), and SP600125 (JNK inhibitor) did not inhibit the activation response of TNF-α on URGCP.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33034821</pmid><doi>10.1007/s10528-020-09972-z</doi><tpages>15</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-2928 |
| ispartof | Biochemical genetics, 2021-02, Vol.59 (1), p.300-314 |
| issn | 0006-2928 1573-4927 |
| language | eng |
| recordid | cdi_proquest_journals_2483427753 |
| source | SpringerLink Journals - AutoHoldings |
| subjects | 1-Phosphatidylinositol 3-kinase Biochemistry Biomedical and Life Sciences Biomedicine Cell cycle Cytokines Cytotoxicity Gene expression Hepatoma Human Genetics Inflammation Inhibitors Liver cancer MAP kinase Medical Microbiology Original Article Proteins Toxicity Transcription Transfection Tumor necrosis factor-α Tumorigenesis Western blotting Wortmannin Zoology |
| title | TNF-α Induces URG-4/URGCP Gene Expression in Hepatoma Cells through Starvation Dependent Manner |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T23%3A49%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TNF-%CE%B1%20Induces%20URG-4/URGCP%20Gene%20Expression%20in%C2%A0Hepatoma%20Cells%20through%20Starvation%20Dependent%20Manner&rft.jtitle=Biochemical%20genetics&rft.au=Tokay,%20Esra&rft.date=2021-02-01&rft.volume=59&rft.issue=1&rft.spage=300&rft.epage=314&rft.pages=300-314&rft.issn=0006-2928&rft.eissn=1573-4927&rft_id=info:doi/10.1007/s10528-020-09972-z&rft_dat=%3Cproquest_cross%3E2483427753%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2483427753&rft_id=info:pmid/33034821&rfr_iscdi=true |