Disulfiram‐copper activates chloride currents and induces apoptosis with tyrosine kinase in prostate cancer cells
Aim: To elucidates the mechanism that disulfiram/copper complex (DSF/Cu) treatment activates chloride channels and induces apoptosis in prostate cancer cells. Methods: Cellular membrane currents were measured by membrane clamp technique; western blot to detect protein expression; flow cytometry to d...
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| Veröffentlicht in: | Asia-Pacific journal of clinical oncology 2022-04, Vol.18 (2), p.e46-e55 |
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| creator | Lei, Wei Xu, Jingkui Ya, Yiyao Zhang, Jinxiang Hou, Xiuying Zhai, Qiliang Zha, Zeyu Zhuo, Yangjia Zhou, You Yuan, Hong Liang, Yuxiang Han, Zhaodong Zhong, Weide Zhu, Linyan Chen, Yehui |
| description | Aim: To elucidates the mechanism that disulfiram/copper complex (DSF/Cu) treatment activates chloride channels and induces apoptosis in prostate cancer cells.
Methods: Cellular membrane currents were measured by membrane clamp technique; western blot to detect protein expression; flow cytometry to detect apoptosis; immunofluorescence to detect target protein co‐localization, and further validated by a combination of protein‐protein interaction and mock protein molecular docking techniques.
Results: DSF/Cu activated chloride channels and induced apoptosis in LNCaP (a type of androgen‐dependent prostate cancer cells) cells. The chloride currents activated by DSF/Cu were significantly reduced after knockdown of CLC3 with siRNA. In addition, DSF/Cu‐activated chloride currents were reduced to background current levels after perfusion with genistein, a highly specific tyrosine kinase inhibitor. Conversely, DSF/Cu failed to activate chloride currents in LNCaP cells after 30 minutes of pre‐incubation with genistein. When genistein was removed, and DSF/Cu was added, the activated currents were small and unstable, and gradually decreased. Immunofluorescence in LNCaP cells also showed co‐localization of the CLC3 protein with tyrosine kinase 2β (PTK2B).
Conclusion: DSF/Cu can activate chloride channels and induce apoptosis in LNCaP cells with the involvement of tyrosine kinase. These results provide new insights into the target therapy of prostate cancer.
DSF/Cu can activate chloride channels of LNCaP cells via tyrosine kinase to generate chloride currents. The activated chloride currents can be inhibited by chloride channel inhibitors DIDS and NPPB. DSF/Cu can effectively promote apoptosis. CLC3 and PYK2B were co‐expressed in LNCaP cells. |
| doi_str_mv | 10.1111/ajco.13551 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9291297</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2491946717</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4481-6c697ff7c36f5b93f42d797c64c58523f56fcf5b5609d6ffefab6e70b23c27363</originalsourceid><addsrcrecordid>eNp9kctOGzEUhq0KVC7tpg9QWWKDkAJje2zHm0oolBaExKZdW84Zu3E6saf2DCi7PgLPyJPgaSBqWdQbX86nT-f4R-gDqU5JWWdmCfGUMM7JG7RPZM0mkgu2sz1zvocOcl5WFVNUkbdojzFRTZUi-yhf-Dy0ziezevz9ALHrbMIGen9nepsxLNqYfGMxDCnZ0GdsQoN9aAYoVdPFro_ZZ3zv-wXu16lcgsU_fTDZFgx35aUvJgwmQDGDbdv8Du0602b7_nk_RN8vP3-bfZ3c3H65mp3fTKCup2QiQCjpnAQmHJ8r5mraSCVB1MCnnDLHhYNS4aJSjXDOOjMXVlZzyoBKJtgh-rTxdsN8ZRso_SfT6i75lUlrHY3X_1aCX-gf8U6Pv0SVLILjZ0GKvwabe73yeRzBBBuHrGmtiKqFJCN69ApdxiGFMp6mkhIhq6mghTrZUFD-JSfrts2QSo9Z6jFL_SfLAn_8u_0t-hJeAcgGuPetXf9Hpc-vZ7cb6RO-yq4F</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2721670862</pqid></control><display><type>article</type><title>Disulfiram‐copper activates chloride currents and induces apoptosis with tyrosine kinase in prostate cancer cells</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Lei, Wei ; Xu, Jingkui ; Ya, Yiyao ; Zhang, Jinxiang ; Hou, Xiuying ; Zhai, Qiliang ; Zha, Zeyu ; Zhuo, Yangjia ; Zhou, You ; Yuan, Hong ; Liang, Yuxiang ; Han, Zhaodong ; Zhong, Weide ; Zhu, Linyan ; Chen, Yehui</creator><creatorcontrib>Lei, Wei ; Xu, Jingkui ; Ya, Yiyao ; Zhang, Jinxiang ; Hou, Xiuying ; Zhai, Qiliang ; Zha, Zeyu ; Zhuo, Yangjia ; Zhou, You ; Yuan, Hong ; Liang, Yuxiang ; Han, Zhaodong ; Zhong, Weide ; Zhu, Linyan ; Chen, Yehui</creatorcontrib><description>Aim: To elucidates the mechanism that disulfiram/copper complex (DSF/Cu) treatment activates chloride channels and induces apoptosis in prostate cancer cells.
Methods: Cellular membrane currents were measured by membrane clamp technique; western blot to detect protein expression; flow cytometry to detect apoptosis; immunofluorescence to detect target protein co‐localization, and further validated by a combination of protein‐protein interaction and mock protein molecular docking techniques.
Results: DSF/Cu activated chloride channels and induced apoptosis in LNCaP (a type of androgen‐dependent prostate cancer cells) cells. The chloride currents activated by DSF/Cu were significantly reduced after knockdown of CLC3 with siRNA. In addition, DSF/Cu‐activated chloride currents were reduced to background current levels after perfusion with genistein, a highly specific tyrosine kinase inhibitor. Conversely, DSF/Cu failed to activate chloride currents in LNCaP cells after 30 minutes of pre‐incubation with genistein. When genistein was removed, and DSF/Cu was added, the activated currents were small and unstable, and gradually decreased. Immunofluorescence in LNCaP cells also showed co‐localization of the CLC3 protein with tyrosine kinase 2β (PTK2B).
Conclusion: DSF/Cu can activate chloride channels and induce apoptosis in LNCaP cells with the involvement of tyrosine kinase. These results provide new insights into the target therapy of prostate cancer.
DSF/Cu can activate chloride channels of LNCaP cells via tyrosine kinase to generate chloride currents. The activated chloride currents can be inhibited by chloride channel inhibitors DIDS and NPPB. DSF/Cu can effectively promote apoptosis. CLC3 and PYK2B were co‐expressed in LNCaP cells.</description><identifier>ISSN: 1743-7555</identifier><identifier>EISSN: 1743-7563</identifier><identifier>DOI: 10.1111/ajco.13551</identifier><identifier>PMID: 33608991</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>Apoptosis ; Cell Line, Tumor ; Cell membranes ; Chloride ; Chloride Channels ; Chloride currents ; Chlorides ; Copper ; Copper - pharmacology ; Disulfiram ; Disulfiram - pharmacology ; DSF/Cu ; Enzyme inhibitors ; Flow cytometry ; Genistein ; Genistein - pharmacology ; Humans ; Immunofluorescence ; Kinases ; Localization ; Male ; Membrane currents ; Molecular Docking Simulation ; Original ; Prostate cancer ; Prostatic Neoplasms - drug therapy ; Protein-tyrosine kinase ; Protein-Tyrosine Kinases ; Proteins ; siRNA ; tyrosine kinase</subject><ispartof>Asia-Pacific journal of clinical oncology, 2022-04, Vol.18 (2), p.e46-e55</ispartof><rights>2021 The Authors. published by John Wiley & Sons Australia, Ltd</rights><rights>2021 The Authors. Asia-Pacific Journal of Clinical Oncology published by John Wiley & Sons Australia, Ltd.</rights><rights>2021. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4481-6c697ff7c36f5b93f42d797c64c58523f56fcf5b5609d6ffefab6e70b23c27363</citedby><cites>FETCH-LOGICAL-c4481-6c697ff7c36f5b93f42d797c64c58523f56fcf5b5609d6ffefab6e70b23c27363</cites><orcidid>0000-0003-0951-2099</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fajco.13551$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fajco.13551$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33608991$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lei, Wei</creatorcontrib><creatorcontrib>Xu, Jingkui</creatorcontrib><creatorcontrib>Ya, Yiyao</creatorcontrib><creatorcontrib>Zhang, Jinxiang</creatorcontrib><creatorcontrib>Hou, Xiuying</creatorcontrib><creatorcontrib>Zhai, Qiliang</creatorcontrib><creatorcontrib>Zha, Zeyu</creatorcontrib><creatorcontrib>Zhuo, Yangjia</creatorcontrib><creatorcontrib>Zhou, You</creatorcontrib><creatorcontrib>Yuan, Hong</creatorcontrib><creatorcontrib>Liang, Yuxiang</creatorcontrib><creatorcontrib>Han, Zhaodong</creatorcontrib><creatorcontrib>Zhong, Weide</creatorcontrib><creatorcontrib>Zhu, Linyan</creatorcontrib><creatorcontrib>Chen, Yehui</creatorcontrib><title>Disulfiram‐copper activates chloride currents and induces apoptosis with tyrosine kinase in prostate cancer cells</title><title>Asia-Pacific journal of clinical oncology</title><addtitle>Asia Pac J Clin Oncol</addtitle><description>Aim: To elucidates the mechanism that disulfiram/copper complex (DSF/Cu) treatment activates chloride channels and induces apoptosis in prostate cancer cells.
Methods: Cellular membrane currents were measured by membrane clamp technique; western blot to detect protein expression; flow cytometry to detect apoptosis; immunofluorescence to detect target protein co‐localization, and further validated by a combination of protein‐protein interaction and mock protein molecular docking techniques.
Results: DSF/Cu activated chloride channels and induced apoptosis in LNCaP (a type of androgen‐dependent prostate cancer cells) cells. The chloride currents activated by DSF/Cu were significantly reduced after knockdown of CLC3 with siRNA. In addition, DSF/Cu‐activated chloride currents were reduced to background current levels after perfusion with genistein, a highly specific tyrosine kinase inhibitor. Conversely, DSF/Cu failed to activate chloride currents in LNCaP cells after 30 minutes of pre‐incubation with genistein. When genistein was removed, and DSF/Cu was added, the activated currents were small and unstable, and gradually decreased. Immunofluorescence in LNCaP cells also showed co‐localization of the CLC3 protein with tyrosine kinase 2β (PTK2B).
Conclusion: DSF/Cu can activate chloride channels and induce apoptosis in LNCaP cells with the involvement of tyrosine kinase. These results provide new insights into the target therapy of prostate cancer.
DSF/Cu can activate chloride channels of LNCaP cells via tyrosine kinase to generate chloride currents. The activated chloride currents can be inhibited by chloride channel inhibitors DIDS and NPPB. DSF/Cu can effectively promote apoptosis. CLC3 and PYK2B were co‐expressed in LNCaP cells.</description><subject>Apoptosis</subject><subject>Cell Line, Tumor</subject><subject>Cell membranes</subject><subject>Chloride</subject><subject>Chloride Channels</subject><subject>Chloride currents</subject><subject>Chlorides</subject><subject>Copper</subject><subject>Copper - pharmacology</subject><subject>Disulfiram</subject><subject>Disulfiram - pharmacology</subject><subject>DSF/Cu</subject><subject>Enzyme inhibitors</subject><subject>Flow cytometry</subject><subject>Genistein</subject><subject>Genistein - pharmacology</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Kinases</subject><subject>Localization</subject><subject>Male</subject><subject>Membrane currents</subject><subject>Molecular Docking Simulation</subject><subject>Original</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Protein-tyrosine kinase</subject><subject>Protein-Tyrosine Kinases</subject><subject>Proteins</subject><subject>siRNA</subject><subject>tyrosine kinase</subject><issn>1743-7555</issn><issn>1743-7563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp9kctOGzEUhq0KVC7tpg9QWWKDkAJje2zHm0oolBaExKZdW84Zu3E6saf2DCi7PgLPyJPgaSBqWdQbX86nT-f4R-gDqU5JWWdmCfGUMM7JG7RPZM0mkgu2sz1zvocOcl5WFVNUkbdojzFRTZUi-yhf-Dy0ziezevz9ALHrbMIGen9nepsxLNqYfGMxDCnZ0GdsQoN9aAYoVdPFro_ZZ3zv-wXu16lcgsU_fTDZFgx35aUvJgwmQDGDbdv8Du0602b7_nk_RN8vP3-bfZ3c3H65mp3fTKCup2QiQCjpnAQmHJ8r5mraSCVB1MCnnDLHhYNS4aJSjXDOOjMXVlZzyoBKJtgh-rTxdsN8ZRso_SfT6i75lUlrHY3X_1aCX-gf8U6Pv0SVLILjZ0GKvwabe73yeRzBBBuHrGmtiKqFJCN69ApdxiGFMp6mkhIhq6mghTrZUFD-JSfrts2QSo9Z6jFL_SfLAn_8u_0t-hJeAcgGuPetXf9Hpc-vZ7cb6RO-yq4F</recordid><startdate>202204</startdate><enddate>202204</enddate><creator>Lei, Wei</creator><creator>Xu, Jingkui</creator><creator>Ya, Yiyao</creator><creator>Zhang, Jinxiang</creator><creator>Hou, Xiuying</creator><creator>Zhai, Qiliang</creator><creator>Zha, Zeyu</creator><creator>Zhuo, Yangjia</creator><creator>Zhou, You</creator><creator>Yuan, Hong</creator><creator>Liang, Yuxiang</creator><creator>Han, Zhaodong</creator><creator>Zhong, Weide</creator><creator>Zhu, Linyan</creator><creator>Chen, Yehui</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</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>7TO</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-0951-2099</orcidid></search><sort><creationdate>202204</creationdate><title>Disulfiram‐copper activates chloride currents and induces apoptosis with tyrosine kinase in prostate cancer cells</title><author>Lei, Wei ; Xu, Jingkui ; Ya, Yiyao ; Zhang, Jinxiang ; Hou, Xiuying ; Zhai, Qiliang ; Zha, Zeyu ; Zhuo, Yangjia ; Zhou, You ; Yuan, Hong ; Liang, Yuxiang ; Han, Zhaodong ; Zhong, Weide ; Zhu, Linyan ; Chen, Yehui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4481-6c697ff7c36f5b93f42d797c64c58523f56fcf5b5609d6ffefab6e70b23c27363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Apoptosis</topic><topic>Cell Line, Tumor</topic><topic>Cell membranes</topic><topic>Chloride</topic><topic>Chloride Channels</topic><topic>Chloride currents</topic><topic>Chlorides</topic><topic>Copper</topic><topic>Copper - pharmacology</topic><topic>Disulfiram</topic><topic>Disulfiram - pharmacology</topic><topic>DSF/Cu</topic><topic>Enzyme inhibitors</topic><topic>Flow cytometry</topic><topic>Genistein</topic><topic>Genistein - pharmacology</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Kinases</topic><topic>Localization</topic><topic>Male</topic><topic>Membrane currents</topic><topic>Molecular Docking Simulation</topic><topic>Original</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Protein-tyrosine kinase</topic><topic>Protein-Tyrosine Kinases</topic><topic>Proteins</topic><topic>siRNA</topic><topic>tyrosine kinase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lei, Wei</creatorcontrib><creatorcontrib>Xu, Jingkui</creatorcontrib><creatorcontrib>Ya, Yiyao</creatorcontrib><creatorcontrib>Zhang, Jinxiang</creatorcontrib><creatorcontrib>Hou, Xiuying</creatorcontrib><creatorcontrib>Zhai, Qiliang</creatorcontrib><creatorcontrib>Zha, Zeyu</creatorcontrib><creatorcontrib>Zhuo, Yangjia</creatorcontrib><creatorcontrib>Zhou, You</creatorcontrib><creatorcontrib>Yuan, Hong</creatorcontrib><creatorcontrib>Liang, Yuxiang</creatorcontrib><creatorcontrib>Han, Zhaodong</creatorcontrib><creatorcontrib>Zhong, Weide</creatorcontrib><creatorcontrib>Zhu, Linyan</creatorcontrib><creatorcontrib>Chen, Yehui</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Asia-Pacific journal of clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lei, Wei</au><au>Xu, Jingkui</au><au>Ya, Yiyao</au><au>Zhang, Jinxiang</au><au>Hou, Xiuying</au><au>Zhai, Qiliang</au><au>Zha, Zeyu</au><au>Zhuo, Yangjia</au><au>Zhou, You</au><au>Yuan, Hong</au><au>Liang, Yuxiang</au><au>Han, Zhaodong</au><au>Zhong, Weide</au><au>Zhu, Linyan</au><au>Chen, Yehui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disulfiram‐copper activates chloride currents and induces apoptosis with tyrosine kinase in prostate cancer cells</atitle><jtitle>Asia-Pacific journal of clinical oncology</jtitle><addtitle>Asia Pac J Clin Oncol</addtitle><date>2022-04</date><risdate>2022</risdate><volume>18</volume><issue>2</issue><spage>e46</spage><epage>e55</epage><pages>e46-e55</pages><issn>1743-7555</issn><eissn>1743-7563</eissn><abstract>Aim: To elucidates the mechanism that disulfiram/copper complex (DSF/Cu) treatment activates chloride channels and induces apoptosis in prostate cancer cells.
Methods: Cellular membrane currents were measured by membrane clamp technique; western blot to detect protein expression; flow cytometry to detect apoptosis; immunofluorescence to detect target protein co‐localization, and further validated by a combination of protein‐protein interaction and mock protein molecular docking techniques.
Results: DSF/Cu activated chloride channels and induced apoptosis in LNCaP (a type of androgen‐dependent prostate cancer cells) cells. The chloride currents activated by DSF/Cu were significantly reduced after knockdown of CLC3 with siRNA. In addition, DSF/Cu‐activated chloride currents were reduced to background current levels after perfusion with genistein, a highly specific tyrosine kinase inhibitor. Conversely, DSF/Cu failed to activate chloride currents in LNCaP cells after 30 minutes of pre‐incubation with genistein. When genistein was removed, and DSF/Cu was added, the activated currents were small and unstable, and gradually decreased. Immunofluorescence in LNCaP cells also showed co‐localization of the CLC3 protein with tyrosine kinase 2β (PTK2B).
Conclusion: DSF/Cu can activate chloride channels and induce apoptosis in LNCaP cells with the involvement of tyrosine kinase. These results provide new insights into the target therapy of prostate cancer.
DSF/Cu can activate chloride channels of LNCaP cells via tyrosine kinase to generate chloride currents. The activated chloride currents can be inhibited by chloride channel inhibitors DIDS and NPPB. DSF/Cu can effectively promote apoptosis. CLC3 and PYK2B were co‐expressed in LNCaP cells.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33608991</pmid><doi>10.1111/ajco.13551</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-0951-2099</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Cell Line, Tumor Cell membranes Chloride Chloride Channels Chloride currents Chlorides Copper Copper - pharmacology Disulfiram Disulfiram - pharmacology DSF/Cu Enzyme inhibitors Flow cytometry Genistein Genistein - pharmacology Humans Immunofluorescence Kinases Localization Male Membrane currents Molecular Docking Simulation Original Prostate cancer Prostatic Neoplasms - drug therapy Protein-tyrosine kinase Protein-Tyrosine Kinases Proteins siRNA tyrosine kinase |
| title | Disulfiram‐copper activates chloride currents and induces apoptosis with tyrosine kinase in prostate cancer cells |
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