Inhibition of TASK-3 (KCNK9) channel biosynthesis changes cell morphology and decreases both DNA content and mitochondrial function of melanoma cells maintained in cell culture

TASK-3 channel overexpression was shown to facilitate the survival of malignantly transformed cells, possibly by providing greater hypoxia tolerance through a still unknown mechanism. Although it has been suggested previously that TASK-3 channels are expressed in the mitochondrial membranes, their r...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Melanoma research 2011-08, Vol.21 (4), p.308-322
Hauptverfasser: Kosztka, Lívia, Rusznák, Zoltán, Nagy, Dénes, Nagy, Zsuzsanna, Fodor, János, Szucs, Géza, Telek, Andrea, Gönczi, Mónika, Ruzsnavszky, Olga, Szentandrássy, Norbert, Csernoch, László
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 322
container_issue 4
container_start_page 308
container_title Melanoma research
container_volume 21
creator Kosztka, Lívia
Rusznák, Zoltán
Nagy, Dénes
Nagy, Zsuzsanna
Fodor, János
Szucs, Géza
Telek, Andrea
Gönczi, Mónika
Ruzsnavszky, Olga
Szentandrássy, Norbert
Csernoch, László
description TASK-3 channel overexpression was shown to facilitate the survival of malignantly transformed cells, possibly by providing greater hypoxia tolerance through a still unknown mechanism. Although it has been suggested previously that TASK-3 channels are expressed in the mitochondrial membranes, their role here remains elusive. In this study, a transient transfection of TASK-3 knockdown melanoma cell cultures was produced to show the significance of TASK-3 expression. Reduction of the TASK-3 protein biosynthesis induced characteristic changes in cell morphology, reduced the amount of DNA and decreased metabolic activity and mitochondrial function of melanoma cells when compared with control. These findings indicate that TASK-3 channel expression and function is indispensable for the proliferation and/or survival of the melanoma cells, as they seem to contribute to their mitochondrial functions. The significance is that, in this study, we have shown that TASK-3 channels are expressed in the mitochondria of melanoma malignum cells, and they are essential for maintaining cellular integrity and viability. The TASK-3 knockdown melanoma cell line had altered morphology, reduced DNA content, decreased metabolic activity and impaired mitochondrial function. These data indicate that TASK-3 channels are functionally present in the mitochondria of the melanoma cells, and their function is essential for the survival of these cells, thus TASK-3 channels may be the possible targets of future anticancer therapy.
doi_str_mv 10.1097/CMR.0b013e3283462713
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_907174880</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>885055817</sourcerecordid><originalsourceid>FETCH-LOGICAL-c338t-58c15354d4815c1a07f39fa9fbc254c7ce39ce4b34f2fb5331d479a3dff214053</originalsourceid><addsrcrecordid>eNqFUcFu1DAQtRAV3S78AUK-0R5S7Iy9to-rpUC1pUhQzpHj2I1RYi-2c9i_4hNJd1sOvXAYPWnem3mjeQi9peSSEiU-bL5-vyQtoWChlsBWtaDwAi0oE1DxFaxeogVRK1JJBfQUneX8ixAqgMMrdFpTTmtGxQL9uQ69b33xMeDo8N36x7YCfL7d3G7VBTa9DsEOuPUx70Ppbfb50Ly3M9phwGNMuz4O8X6PdehwZ02yOs9sG0uPP96usYmh2FAO9OhLNH0MXfJ6wG4K5sl4tIMOcdSHrRmP2ocyl-2wD0cnMw1lSvY1OnF6yPbNIy7Rz09Xd5sv1c23z9eb9U1lAGSpuDSUA2cdk5QbqolwoJxWrjU1Z0YYC8pY1gJztWs5AO2YUBo652rKCIclen_cu0vx92RzaUafHw7RwcYpN4oIKpiU5L9KKTnhXM6_XyJ2VJoUc07WNbvkR532DSXNQ6jNHGrzPNR57N2jwdSOtvs39JQi_AVaop-s</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>885055817</pqid></control><display><type>article</type><title>Inhibition of TASK-3 (KCNK9) channel biosynthesis changes cell morphology and decreases both DNA content and mitochondrial function of melanoma cells maintained in cell culture</title><source>MEDLINE</source><source>Journals@Ovid Complete</source><creator>Kosztka, Lívia ; Rusznák, Zoltán ; Nagy, Dénes ; Nagy, Zsuzsanna ; Fodor, János ; Szucs, Géza ; Telek, Andrea ; Gönczi, Mónika ; Ruzsnavszky, Olga ; Szentandrássy, Norbert ; Csernoch, László</creator><creatorcontrib>Kosztka, Lívia ; Rusznák, Zoltán ; Nagy, Dénes ; Nagy, Zsuzsanna ; Fodor, János ; Szucs, Géza ; Telek, Andrea ; Gönczi, Mónika ; Ruzsnavszky, Olga ; Szentandrássy, Norbert ; Csernoch, László</creatorcontrib><description>TASK-3 channel overexpression was shown to facilitate the survival of malignantly transformed cells, possibly by providing greater hypoxia tolerance through a still unknown mechanism. Although it has been suggested previously that TASK-3 channels are expressed in the mitochondrial membranes, their role here remains elusive. In this study, a transient transfection of TASK-3 knockdown melanoma cell cultures was produced to show the significance of TASK-3 expression. Reduction of the TASK-3 protein biosynthesis induced characteristic changes in cell morphology, reduced the amount of DNA and decreased metabolic activity and mitochondrial function of melanoma cells when compared with control. These findings indicate that TASK-3 channel expression and function is indispensable for the proliferation and/or survival of the melanoma cells, as they seem to contribute to their mitochondrial functions. The significance is that, in this study, we have shown that TASK-3 channels are expressed in the mitochondria of melanoma malignum cells, and they are essential for maintaining cellular integrity and viability. The TASK-3 knockdown melanoma cell line had altered morphology, reduced DNA content, decreased metabolic activity and impaired mitochondrial function. These data indicate that TASK-3 channels are functionally present in the mitochondria of the melanoma cells, and their function is essential for the survival of these cells, thus TASK-3 channels may be the possible targets of future anticancer therapy.</description><identifier>ISSN: 0960-8931</identifier><identifier>EISSN: 1473-5636</identifier><identifier>DOI: 10.1097/CMR.0b013e3283462713</identifier><identifier>PMID: 21512417</identifier><language>eng</language><publisher>England</publisher><subject>Cell Line, Tumor ; Cell Proliferation ; Cell Shape ; Cell Size ; Cell Survival ; DNA - metabolism ; Energy Metabolism ; HEK293 Cells ; Humans ; Melanoma - genetics ; Melanoma - metabolism ; Melanoma - pathology ; Mitochondria - metabolism ; Mitochondria - pathology ; Potassium Channels, Tandem Pore Domain - biosynthesis ; Potassium Channels, Tandem Pore Domain - genetics ; RNA Interference ; Time Factors ; Transfection</subject><ispartof>Melanoma research, 2011-08, Vol.21 (4), p.308-322</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c338t-58c15354d4815c1a07f39fa9fbc254c7ce39ce4b34f2fb5331d479a3dff214053</citedby><cites>FETCH-LOGICAL-c338t-58c15354d4815c1a07f39fa9fbc254c7ce39ce4b34f2fb5331d479a3dff214053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21512417$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kosztka, Lívia</creatorcontrib><creatorcontrib>Rusznák, Zoltán</creatorcontrib><creatorcontrib>Nagy, Dénes</creatorcontrib><creatorcontrib>Nagy, Zsuzsanna</creatorcontrib><creatorcontrib>Fodor, János</creatorcontrib><creatorcontrib>Szucs, Géza</creatorcontrib><creatorcontrib>Telek, Andrea</creatorcontrib><creatorcontrib>Gönczi, Mónika</creatorcontrib><creatorcontrib>Ruzsnavszky, Olga</creatorcontrib><creatorcontrib>Szentandrássy, Norbert</creatorcontrib><creatorcontrib>Csernoch, László</creatorcontrib><title>Inhibition of TASK-3 (KCNK9) channel biosynthesis changes cell morphology and decreases both DNA content and mitochondrial function of melanoma cells maintained in cell culture</title><title>Melanoma research</title><addtitle>Melanoma Res</addtitle><description>TASK-3 channel overexpression was shown to facilitate the survival of malignantly transformed cells, possibly by providing greater hypoxia tolerance through a still unknown mechanism. Although it has been suggested previously that TASK-3 channels are expressed in the mitochondrial membranes, their role here remains elusive. In this study, a transient transfection of TASK-3 knockdown melanoma cell cultures was produced to show the significance of TASK-3 expression. Reduction of the TASK-3 protein biosynthesis induced characteristic changes in cell morphology, reduced the amount of DNA and decreased metabolic activity and mitochondrial function of melanoma cells when compared with control. These findings indicate that TASK-3 channel expression and function is indispensable for the proliferation and/or survival of the melanoma cells, as they seem to contribute to their mitochondrial functions. The significance is that, in this study, we have shown that TASK-3 channels are expressed in the mitochondria of melanoma malignum cells, and they are essential for maintaining cellular integrity and viability. The TASK-3 knockdown melanoma cell line had altered morphology, reduced DNA content, decreased metabolic activity and impaired mitochondrial function. These data indicate that TASK-3 channels are functionally present in the mitochondria of the melanoma cells, and their function is essential for the survival of these cells, thus TASK-3 channels may be the possible targets of future anticancer therapy.</description><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Shape</subject><subject>Cell Size</subject><subject>Cell Survival</subject><subject>DNA - metabolism</subject><subject>Energy Metabolism</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Potassium Channels, Tandem Pore Domain - biosynthesis</subject><subject>Potassium Channels, Tandem Pore Domain - genetics</subject><subject>RNA Interference</subject><subject>Time Factors</subject><subject>Transfection</subject><issn>0960-8931</issn><issn>1473-5636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUcFu1DAQtRAV3S78AUK-0R5S7Iy9to-rpUC1pUhQzpHj2I1RYi-2c9i_4hNJd1sOvXAYPWnem3mjeQi9peSSEiU-bL5-vyQtoWChlsBWtaDwAi0oE1DxFaxeogVRK1JJBfQUneX8ixAqgMMrdFpTTmtGxQL9uQ69b33xMeDo8N36x7YCfL7d3G7VBTa9DsEOuPUx70Ppbfb50Ly3M9phwGNMuz4O8X6PdehwZ02yOs9sG0uPP96usYmh2FAO9OhLNH0MXfJ6wG4K5sl4tIMOcdSHrRmP2ocyl-2wD0cnMw1lSvY1OnF6yPbNIy7Rz09Xd5sv1c23z9eb9U1lAGSpuDSUA2cdk5QbqolwoJxWrjU1Z0YYC8pY1gJztWs5AO2YUBo652rKCIclen_cu0vx92RzaUafHw7RwcYpN4oIKpiU5L9KKTnhXM6_XyJ2VJoUc07WNbvkR532DSXNQ6jNHGrzPNR57N2jwdSOtvs39JQi_AVaop-s</recordid><startdate>201108</startdate><enddate>201108</enddate><creator>Kosztka, Lívia</creator><creator>Rusznák, Zoltán</creator><creator>Nagy, Dénes</creator><creator>Nagy, Zsuzsanna</creator><creator>Fodor, János</creator><creator>Szucs, Géza</creator><creator>Telek, Andrea</creator><creator>Gönczi, Mónika</creator><creator>Ruzsnavszky, Olga</creator><creator>Szentandrássy, Norbert</creator><creator>Csernoch, László</creator><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>7X8</scope><scope>7QO</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>201108</creationdate><title>Inhibition of TASK-3 (KCNK9) channel biosynthesis changes cell morphology and decreases both DNA content and mitochondrial function of melanoma cells maintained in cell culture</title><author>Kosztka, Lívia ; Rusznák, Zoltán ; Nagy, Dénes ; Nagy, Zsuzsanna ; Fodor, János ; Szucs, Géza ; Telek, Andrea ; Gönczi, Mónika ; Ruzsnavszky, Olga ; Szentandrássy, Norbert ; Csernoch, László</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c338t-58c15354d4815c1a07f39fa9fbc254c7ce39ce4b34f2fb5331d479a3dff214053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Shape</topic><topic>Cell Size</topic><topic>Cell Survival</topic><topic>DNA - metabolism</topic><topic>Energy Metabolism</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Melanoma - genetics</topic><topic>Melanoma - metabolism</topic><topic>Melanoma - pathology</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - pathology</topic><topic>Potassium Channels, Tandem Pore Domain - biosynthesis</topic><topic>Potassium Channels, Tandem Pore Domain - genetics</topic><topic>RNA Interference</topic><topic>Time Factors</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kosztka, Lívia</creatorcontrib><creatorcontrib>Rusznák, Zoltán</creatorcontrib><creatorcontrib>Nagy, Dénes</creatorcontrib><creatorcontrib>Nagy, Zsuzsanna</creatorcontrib><creatorcontrib>Fodor, János</creatorcontrib><creatorcontrib>Szucs, Géza</creatorcontrib><creatorcontrib>Telek, Andrea</creatorcontrib><creatorcontrib>Gönczi, Mónika</creatorcontrib><creatorcontrib>Ruzsnavszky, Olga</creatorcontrib><creatorcontrib>Szentandrássy, Norbert</creatorcontrib><creatorcontrib>Csernoch, László</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Melanoma research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kosztka, Lívia</au><au>Rusznák, Zoltán</au><au>Nagy, Dénes</au><au>Nagy, Zsuzsanna</au><au>Fodor, János</au><au>Szucs, Géza</au><au>Telek, Andrea</au><au>Gönczi, Mónika</au><au>Ruzsnavszky, Olga</au><au>Szentandrássy, Norbert</au><au>Csernoch, László</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of TASK-3 (KCNK9) channel biosynthesis changes cell morphology and decreases both DNA content and mitochondrial function of melanoma cells maintained in cell culture</atitle><jtitle>Melanoma research</jtitle><addtitle>Melanoma Res</addtitle><date>2011-08</date><risdate>2011</risdate><volume>21</volume><issue>4</issue><spage>308</spage><epage>322</epage><pages>308-322</pages><issn>0960-8931</issn><eissn>1473-5636</eissn><abstract>TASK-3 channel overexpression was shown to facilitate the survival of malignantly transformed cells, possibly by providing greater hypoxia tolerance through a still unknown mechanism. Although it has been suggested previously that TASK-3 channels are expressed in the mitochondrial membranes, their role here remains elusive. In this study, a transient transfection of TASK-3 knockdown melanoma cell cultures was produced to show the significance of TASK-3 expression. Reduction of the TASK-3 protein biosynthesis induced characteristic changes in cell morphology, reduced the amount of DNA and decreased metabolic activity and mitochondrial function of melanoma cells when compared with control. These findings indicate that TASK-3 channel expression and function is indispensable for the proliferation and/or survival of the melanoma cells, as they seem to contribute to their mitochondrial functions. The significance is that, in this study, we have shown that TASK-3 channels are expressed in the mitochondria of melanoma malignum cells, and they are essential for maintaining cellular integrity and viability. The TASK-3 knockdown melanoma cell line had altered morphology, reduced DNA content, decreased metabolic activity and impaired mitochondrial function. These data indicate that TASK-3 channels are functionally present in the mitochondria of the melanoma cells, and their function is essential for the survival of these cells, thus TASK-3 channels may be the possible targets of future anticancer therapy.</abstract><cop>England</cop><pmid>21512417</pmid><doi>10.1097/CMR.0b013e3283462713</doi><tpages>15</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0960-8931
ispartof Melanoma research, 2011-08, Vol.21 (4), p.308-322
issn 0960-8931
1473-5636
language eng
recordid cdi_proquest_miscellaneous_907174880
source MEDLINE; Journals@Ovid Complete
subjects Cell Line, Tumor
Cell Proliferation
Cell Shape
Cell Size
Cell Survival
DNA - metabolism
Energy Metabolism
HEK293 Cells
Humans
Melanoma - genetics
Melanoma - metabolism
Melanoma - pathology
Mitochondria - metabolism
Mitochondria - pathology
Potassium Channels, Tandem Pore Domain - biosynthesis
Potassium Channels, Tandem Pore Domain - genetics
RNA Interference
Time Factors
Transfection
title Inhibition of TASK-3 (KCNK9) channel biosynthesis changes cell morphology and decreases both DNA content and mitochondrial function of melanoma cells maintained in cell culture
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-20T08%3A13%3A20IST&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=Inhibition%20of%20TASK-3%20(KCNK9)%20channel%20biosynthesis%20changes%20cell%20morphology%20and%20decreases%20both%20DNA%20content%20and%20mitochondrial%20function%20of%20melanoma%20cells%20maintained%20in%20cell%20culture&rft.jtitle=Melanoma%20research&rft.au=Kosztka,%20L%C3%ADvia&rft.date=2011-08&rft.volume=21&rft.issue=4&rft.spage=308&rft.epage=322&rft.pages=308-322&rft.issn=0960-8931&rft.eissn=1473-5636&rft_id=info:doi/10.1097/CMR.0b013e3283462713&rft_dat=%3Cproquest_cross%3E885055817%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=885055817&rft_id=info:pmid/21512417&rfr_iscdi=true