Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells
Pathophysiological functions of chloride intracellular channel protein 3 (CLIC3) in human gastric cancer have been unclear. In the tissue microarray analysis using 107 gastric cancer specimens, CLIC3 expression was negatively correlated with pathological tumor depth, and the patients with lower expr...
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description | Pathophysiological functions of chloride intracellular channel protein 3 (CLIC3) in human gastric cancer have been unclear. In the tissue microarray analysis using 107 gastric cancer specimens, CLIC3 expression was negatively correlated with pathological tumor depth, and the patients with lower expression of CLIC3 exhibited poorer prognosis. CLIC3 was expressed in the plasma membrane of cancer cells in the tissue. CLIC3 expression was also found in a human gastric cancer cell line (MKN7). In whole-cell patch-clamp recordings of the cells expressing CLIC3, NPPB-sensitive outwardly rectifying Cl− currents were observed. Cell proliferation was significantly accelerated by knockdown of CLIC3 in MKN7 cells. On the other hand, the proliferation was attenuated by exogenous CLIC3 expression in human gastric cancer cells (KATOIII and NUGC-4) in which endogenous CLIC3 expression is negligible. Our results suggest that CLIC3 functions as a Cl− channel in the plasma membrane of gastric cancer cells and that decreased expression of CLIC3 results in unfavorable prognosis of gastric cancer patients. |
doi_str_mv | 10.1186/s12576-020-00740-7 |
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In the tissue microarray analysis using 107 gastric cancer specimens, CLIC3 expression was negatively correlated with pathological tumor depth, and the patients with lower expression of CLIC3 exhibited poorer prognosis. CLIC3 was expressed in the plasma membrane of cancer cells in the tissue. CLIC3 expression was also found in a human gastric cancer cell line (MKN7). In whole-cell patch-clamp recordings of the cells expressing CLIC3, NPPB-sensitive outwardly rectifying Cl− currents were observed. Cell proliferation was significantly accelerated by knockdown of CLIC3 in MKN7 cells. On the other hand, the proliferation was attenuated by exogenous CLIC3 expression in human gastric cancer cells (KATOIII and NUGC-4) in which endogenous CLIC3 expression is negligible. Our results suggest that CLIC3 functions as a Cl− channel in the plasma membrane of gastric cancer cells and that decreased expression of CLIC3 results in unfavorable prognosis of gastric cancer patients.</description><identifier>ISSN: 1880-6546</identifier><identifier>EISSN: 1880-6562</identifier><identifier>DOI: 10.1186/s12576-020-00740-7</identifier><identifier>PMID: 32066374</identifier><language>eng</language><publisher>Japan: Elsevier Inc</publisher><subject>Analysis ; Antibiotics ; Antibodies ; Cancer ; Cancer cells ; Cancer therapies ; Cell Line, Tumor ; Cell Migration Assays ; Cell Proliferation ; Chloride ; Chloride channel ; Chloride Channels - genetics ; Chloride Channels - metabolism ; Chloride intracellular channel protein ; Chlorides ; Cloning, Molecular ; DNA microarrays ; DNA polymerase ; Gastric cancer ; Gene Expression Regulation, Neoplastic ; Humans ; Medical research ; Membrane Potentials - physiology ; Original Paper ; Patch-Clamp Techniques ; Prognosis ; Proteins ; Software ; Stomach cancer ; Stomach Neoplasms ; Tumors</subject><ispartof>The journal of physiological sciences, 2020-02, Vol.70 (1), p.15-15, Article 15</ispartof><rights>2020 The Author(s)</rights><rights>COPYRIGHT 2020 Springer</rights><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>The Author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c678t-5e00fc1b91e84324aa9448ad040bea5f60d7daedead01773cae0b9f06d6cc1753</citedby><cites>FETCH-LOGICAL-c678t-5e00fc1b91e84324aa9448ad040bea5f60d7daedead01773cae0b9f06d6cc1753</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/PMC7026216/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026216/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32066374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kawai, Shunsuke</creatorcontrib><creatorcontrib>Fujii, Takuto</creatorcontrib><creatorcontrib>Shimizu, Takahiro</creatorcontrib><creatorcontrib>Sukegawa, Kenta</creatorcontrib><creatorcontrib>Hashimoto, Isaya</creatorcontrib><creatorcontrib>Okumura, Tomoyuki</creatorcontrib><creatorcontrib>Nagata, Takuya</creatorcontrib><creatorcontrib>Sakai, Hideki</creatorcontrib><creatorcontrib>Fujii, Tsutomu</creatorcontrib><title>Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells</title><title>The journal of physiological sciences</title><addtitle>J Physiol Sci</addtitle><description>Pathophysiological functions of chloride intracellular channel protein 3 (CLIC3) in human gastric cancer have been unclear. In the tissue microarray analysis using 107 gastric cancer specimens, CLIC3 expression was negatively correlated with pathological tumor depth, and the patients with lower expression of CLIC3 exhibited poorer prognosis. CLIC3 was expressed in the plasma membrane of cancer cells in the tissue. CLIC3 expression was also found in a human gastric cancer cell line (MKN7). In whole-cell patch-clamp recordings of the cells expressing CLIC3, NPPB-sensitive outwardly rectifying Cl− currents were observed. Cell proliferation was significantly accelerated by knockdown of CLIC3 in MKN7 cells. On the other hand, the proliferation was attenuated by exogenous CLIC3 expression in human gastric cancer cells (KATOIII and NUGC-4) in which endogenous CLIC3 expression is negligible. Our results suggest that CLIC3 functions as a Cl− channel in the plasma membrane of gastric cancer cells and that decreased expression of CLIC3 results in unfavorable prognosis of gastric cancer patients.</description><subject>Analysis</subject><subject>Antibiotics</subject><subject>Antibodies</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Cell Line, Tumor</subject><subject>Cell Migration Assays</subject><subject>Cell Proliferation</subject><subject>Chloride</subject><subject>Chloride channel</subject><subject>Chloride Channels - genetics</subject><subject>Chloride Channels - metabolism</subject><subject>Chloride intracellular channel protein</subject><subject>Chlorides</subject><subject>Cloning, Molecular</subject><subject>DNA microarrays</subject><subject>DNA polymerase</subject><subject>Gastric cancer</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Medical research</subject><subject>Membrane Potentials - physiology</subject><subject>Original Paper</subject><subject>Patch-Clamp Techniques</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Software</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms</subject><subject>Tumors</subject><issn>1880-6546</issn><issn>1880-6562</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</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><recordid>eNp9kk1v1DAQhiMEoh_wBzigSFy4pIwdf2QlhFStoFRaCQ70bHntSeIqsYOdVOq_r5ctC0Ur5INH9jOvPTNvUbwhcEFIIz4kQrkUFVCoACSDSj4rTknTQCW4oM8PMRMnxVlKtwBMrGjzsjipKQhRS3Za3HzXcx-m_j65MITOGT2UUwwTxtlhKkNbrjfX67o0_RCis5gD7T0OpfNlv4zal51Oc3SmNNobjKXBYUivihetHhK-ftzPi5svn3-sv1abb1fX68tNZYRs5oojQGvIdkWwYTVlWq8Ya7QFBlvUvBVgpdVoMR8RKWujEbarFoQVxhDJ6_Pi0153WrYjWoN-jnpQU3SjjvcqaKee3njXqy7cKQlUUCKywPtHgRh-LphmNbq0K0F7DEtStOaScc5JndF3_6C3YYk-l6coZxI4W3H5h-r0gMr5NuR3zU5UXUrB64wKmqnqCNWhx_zJ4LF1-fgJf3GEz8vi6MzRBLpPMDGkFLE99ISA2plH7c2jsnnUL_Oo3d_f_t3NQ8pvt2Tg4x7APNM7h1El4zCP3bqIZlY2uP_pPwDtodJf</recordid><startdate>20200217</startdate><enddate>20200217</enddate><creator>Kawai, Shunsuke</creator><creator>Fujii, Takuto</creator><creator>Shimizu, Takahiro</creator><creator>Sukegawa, Kenta</creator><creator>Hashimoto, Isaya</creator><creator>Okumura, Tomoyuki</creator><creator>Nagata, Takuya</creator><creator>Sakai, Hideki</creator><creator>Fujii, Tsutomu</creator><general>Elsevier Inc</general><general>Springer</general><general>BioMed Central</general><scope>6I.</scope><scope>AAFTH</scope><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>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200217</creationdate><title>Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells</title><author>Kawai, Shunsuke ; 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In the tissue microarray analysis using 107 gastric cancer specimens, CLIC3 expression was negatively correlated with pathological tumor depth, and the patients with lower expression of CLIC3 exhibited poorer prognosis. CLIC3 was expressed in the plasma membrane of cancer cells in the tissue. CLIC3 expression was also found in a human gastric cancer cell line (MKN7). In whole-cell patch-clamp recordings of the cells expressing CLIC3, NPPB-sensitive outwardly rectifying Cl− currents were observed. Cell proliferation was significantly accelerated by knockdown of CLIC3 in MKN7 cells. On the other hand, the proliferation was attenuated by exogenous CLIC3 expression in human gastric cancer cells (KATOIII and NUGC-4) in which endogenous CLIC3 expression is negligible. Our results suggest that CLIC3 functions as a Cl− channel in the plasma membrane of gastric cancer cells and that decreased expression of CLIC3 results in unfavorable prognosis of gastric cancer patients.</abstract><cop>Japan</cop><pub>Elsevier Inc</pub><pmid>32066374</pmid><doi>10.1186/s12576-020-00740-7</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Antibiotics Antibodies Cancer Cancer cells Cancer therapies Cell Line, Tumor Cell Migration Assays Cell Proliferation Chloride Chloride channel Chloride Channels - genetics Chloride Channels - metabolism Chloride intracellular channel protein Chlorides Cloning, Molecular DNA microarrays DNA polymerase Gastric cancer Gene Expression Regulation, Neoplastic Humans Medical research Membrane Potentials - physiology Original Paper Patch-Clamp Techniques Prognosis Proteins Software Stomach cancer Stomach Neoplasms Tumors |
title | Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells |
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