Inhibition of sorcin reverses multidrug resistance of K562/A02 cells and MCF-7/A02 cells via regulating apoptosis-related proteins
Purpose Sorcin, a 22-kDa calcium-binding protein, renders cancer cells resistant to chemotherapeutic agents, thus playing an important role in multidrug resistance (MDR). But the mechanisms mediated by sorcin still remain quite elusive. This study aim to explore whether sorcin silencing could restor...
Gespeichert in:
| Veröffentlicht in: | Cancer chemotherapy and pharmacology 2013-10, Vol.72 (4), p.789-798 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 798 |
|---|---|
| container_issue | 4 |
| container_start_page | 789 |
| container_title | Cancer chemotherapy and pharmacology |
| container_volume | 72 |
| creator | Hu, Yunhui Cheng, Xin Li, Shuangjing Zhou, Yuan Wang, Jianxiang Cheng, Tao Yang, Ming Xiong, Dongsheng |
| description | Purpose
Sorcin, a 22-kDa calcium-binding protein, renders cancer cells resistant to chemotherapeutic agents, thus playing an important role in multidrug resistance (MDR). But the mechanisms mediated by sorcin still remain quite elusive. This study aim to explore whether sorcin silencing could restore chemosensitivity in MDR cancer cells and seek to identify the functional mechanisms mediated by sorcin.
Methods
To investigate the mechanisms of sorcin-silencing-induced chemosensitivity, transient expression of sorcin-siRNAs was performed in doxorubicin-induced MDR cell lines, K562/A02 and MCF-7/A02. Sensitivity to five chemotherapeutic agents was evaluated by analysis of cell survival and cell apoptosis.
Results
In this report, we show that down-regulation of sorcin did not alter expression or function of P-gp, but actually induced cell apoptosis and chemosensitivity in K562/A02 and MCF-7/A02. We also observe that silencing of sorcin-enhanced chemotherapeutic agent effects partly through regulating apoptosis-related protein, including Bcl-2, Bax, c-jun and c-fos.
Conclusion
This offers the rationale for the development of therapeutic strategies down-regulating sorcin expression for the treatment of cancer, especially for the reversal of MDR. |
| doi_str_mv | 10.1007/s00280-013-2254-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1437578226</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3082013541</sourcerecordid><originalsourceid>FETCH-LOGICAL-c468t-2f0238a18466894a089617aa9c88278d9555410074e79f9c16d9ca77dc28a3003</originalsourceid><addsrcrecordid>eNp1kV9rFDEUxYNY7Lr6AXyRARF8SXuTyb95LEurxZa-6HNIM5k1ZTZZc2cKvvrJzbCrFsGnwM3v3Hs4h5A3DM4YgD5HAG6AAmsp51JQ_oysmGg5BSPa52QFrRBUahCn5CXiAwAI1rYvyCkXVSO1XJGf1-lbvI9TzKnJQ4O5-JiaEh5DwYDNbh6n2Jd5W0cYcXLJh4X7LBU_vwDe-DCO2LjUN7ebK6qfzB6jq6LtPLoppm3j9nk_5bqDllBHoW_2JU8hJnxFTgY3Ynh9fNfk69Xll80nenP38XpzcUO9UGaifADeGseMUMp0woHpFNPOdd4Yrk3fSSnFEosIuhs6z1Tfead177lxLUC7Jh8Oe-vh73PAye4iLl5dCnlGW5PTUhvOVUXf_YM-5Lmk6m6hlFKcSV0pdqB8yYglDHZf4s6VH5aBXZzYQ0G2hm2XgiyvmrfHzfP9LvR_FL8bqcD7I-DQu3EoNfKIfzmtdcdqi2vCDxzWr7QN5YnF_17_BRREpXM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1436662157</pqid></control><display><type>article</type><title>Inhibition of sorcin reverses multidrug resistance of K562/A02 cells and MCF-7/A02 cells via regulating apoptosis-related proteins</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Hu, Yunhui ; Cheng, Xin ; Li, Shuangjing ; Zhou, Yuan ; Wang, Jianxiang ; Cheng, Tao ; Yang, Ming ; Xiong, Dongsheng</creator><creatorcontrib>Hu, Yunhui ; Cheng, Xin ; Li, Shuangjing ; Zhou, Yuan ; Wang, Jianxiang ; Cheng, Tao ; Yang, Ming ; Xiong, Dongsheng</creatorcontrib><description>Purpose
Sorcin, a 22-kDa calcium-binding protein, renders cancer cells resistant to chemotherapeutic agents, thus playing an important role in multidrug resistance (MDR). But the mechanisms mediated by sorcin still remain quite elusive. This study aim to explore whether sorcin silencing could restore chemosensitivity in MDR cancer cells and seek to identify the functional mechanisms mediated by sorcin.
Methods
To investigate the mechanisms of sorcin-silencing-induced chemosensitivity, transient expression of sorcin-siRNAs was performed in doxorubicin-induced MDR cell lines, K562/A02 and MCF-7/A02. Sensitivity to five chemotherapeutic agents was evaluated by analysis of cell survival and cell apoptosis.
Results
In this report, we show that down-regulation of sorcin did not alter expression or function of P-gp, but actually induced cell apoptosis and chemosensitivity in K562/A02 and MCF-7/A02. We also observe that silencing of sorcin-enhanced chemotherapeutic agent effects partly through regulating apoptosis-related protein, including Bcl-2, Bax, c-jun and c-fos.
Conclusion
This offers the rationale for the development of therapeutic strategies down-regulating sorcin expression for the treatment of cancer, especially for the reversal of MDR.</description><identifier>ISSN: 0344-5704</identifier><identifier>EISSN: 1432-0843</identifier><identifier>DOI: 10.1007/s00280-013-2254-2</identifier><identifier>PMID: 24013575</identifier><identifier>CODEN: CCPHDZ</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Antineoplastic agents ; Antineoplastic Agents - pharmacology ; Apoptosis - drug effects ; ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism ; Biological and medical sciences ; Breast Neoplasms - drug therapy ; Calcium-Binding Proteins - genetics ; Cancer Research ; Cell Survival - drug effects ; Down-Regulation ; Doxorubicin - pharmacology ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm - genetics ; Female ; Gene Silencing ; Humans ; K562 Cells ; Leukemia - drug therapy ; MCF-7 Cells ; Medical sciences ; Medicine ; Medicine & Public Health ; Oncology ; Original Article ; Pharmacology. Drug treatments ; Pharmacology/Toxicology ; RNA, Small Interfering - administration & dosage</subject><ispartof>Cancer chemotherapy and pharmacology, 2013-10, Vol.72 (4), p.789-798</ispartof><rights>Springer-Verlag Berlin Heidelberg 2013</rights><rights>2014 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-2f0238a18466894a089617aa9c88278d9555410074e79f9c16d9ca77dc28a3003</citedby><cites>FETCH-LOGICAL-c468t-2f0238a18466894a089617aa9c88278d9555410074e79f9c16d9ca77dc28a3003</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/s00280-013-2254-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00280-013-2254-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27779113$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24013575$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Yunhui</creatorcontrib><creatorcontrib>Cheng, Xin</creatorcontrib><creatorcontrib>Li, Shuangjing</creatorcontrib><creatorcontrib>Zhou, Yuan</creatorcontrib><creatorcontrib>Wang, Jianxiang</creatorcontrib><creatorcontrib>Cheng, Tao</creatorcontrib><creatorcontrib>Yang, Ming</creatorcontrib><creatorcontrib>Xiong, Dongsheng</creatorcontrib><title>Inhibition of sorcin reverses multidrug resistance of K562/A02 cells and MCF-7/A02 cells via regulating apoptosis-related proteins</title><title>Cancer chemotherapy and pharmacology</title><addtitle>Cancer Chemother Pharmacol</addtitle><addtitle>Cancer Chemother Pharmacol</addtitle><description>Purpose
Sorcin, a 22-kDa calcium-binding protein, renders cancer cells resistant to chemotherapeutic agents, thus playing an important role in multidrug resistance (MDR). But the mechanisms mediated by sorcin still remain quite elusive. This study aim to explore whether sorcin silencing could restore chemosensitivity in MDR cancer cells and seek to identify the functional mechanisms mediated by sorcin.
Methods
To investigate the mechanisms of sorcin-silencing-induced chemosensitivity, transient expression of sorcin-siRNAs was performed in doxorubicin-induced MDR cell lines, K562/A02 and MCF-7/A02. Sensitivity to five chemotherapeutic agents was evaluated by analysis of cell survival and cell apoptosis.
Results
In this report, we show that down-regulation of sorcin did not alter expression or function of P-gp, but actually induced cell apoptosis and chemosensitivity in K562/A02 and MCF-7/A02. We also observe that silencing of sorcin-enhanced chemotherapeutic agent effects partly through regulating apoptosis-related protein, including Bcl-2, Bax, c-jun and c-fos.
Conclusion
This offers the rationale for the development of therapeutic strategies down-regulating sorcin expression for the treatment of cancer, especially for the reversal of MDR.</description><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism</subject><subject>Biological and medical sciences</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Cancer Research</subject><subject>Cell Survival - drug effects</subject><subject>Down-Regulation</subject><subject>Doxorubicin - pharmacology</subject><subject>Drug Resistance, Multiple</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>K562 Cells</subject><subject>Leukemia - drug therapy</subject><subject>MCF-7 Cells</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pharmacology. Drug treatments</subject><subject>Pharmacology/Toxicology</subject><subject>RNA, Small Interfering - administration & dosage</subject><issn>0344-5704</issn><issn>1432-0843</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kV9rFDEUxYNY7Lr6AXyRARF8SXuTyb95LEurxZa-6HNIM5k1ZTZZc2cKvvrJzbCrFsGnwM3v3Hs4h5A3DM4YgD5HAG6AAmsp51JQ_oysmGg5BSPa52QFrRBUahCn5CXiAwAI1rYvyCkXVSO1XJGf1-lbvI9TzKnJQ4O5-JiaEh5DwYDNbh6n2Jd5W0cYcXLJh4X7LBU_vwDe-DCO2LjUN7ebK6qfzB6jq6LtPLoppm3j9nk_5bqDllBHoW_2JU8hJnxFTgY3Ynh9fNfk69Xll80nenP38XpzcUO9UGaifADeGseMUMp0woHpFNPOdd4Yrk3fSSnFEosIuhs6z1Tfead177lxLUC7Jh8Oe-vh73PAye4iLl5dCnlGW5PTUhvOVUXf_YM-5Lmk6m6hlFKcSV0pdqB8yYglDHZf4s6VH5aBXZzYQ0G2hm2XgiyvmrfHzfP9LvR_FL8bqcD7I-DQu3EoNfKIfzmtdcdqi2vCDxzWr7QN5YnF_17_BRREpXM</recordid><startdate>20131001</startdate><enddate>20131001</enddate><creator>Hu, Yunhui</creator><creator>Cheng, Xin</creator><creator>Li, Shuangjing</creator><creator>Zhou, Yuan</creator><creator>Wang, Jianxiang</creator><creator>Cheng, Tao</creator><creator>Yang, Ming</creator><creator>Xiong, Dongsheng</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</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>20131001</creationdate><title>Inhibition of sorcin reverses multidrug resistance of K562/A02 cells and MCF-7/A02 cells via regulating apoptosis-related proteins</title><author>Hu, Yunhui ; Cheng, Xin ; Li, Shuangjing ; Zhou, Yuan ; Wang, Jianxiang ; Cheng, Tao ; Yang, Ming ; Xiong, Dongsheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-2f0238a18466894a089617aa9c88278d9555410074e79f9c16d9ca77dc28a3003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism</topic><topic>Biological and medical sciences</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Cancer Research</topic><topic>Cell Survival - drug effects</topic><topic>Down-Regulation</topic><topic>Doxorubicin - pharmacology</topic><topic>Drug Resistance, Multiple</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Female</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>K562 Cells</topic><topic>Leukemia - drug therapy</topic><topic>MCF-7 Cells</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pharmacology. Drug treatments</topic><topic>Pharmacology/Toxicology</topic><topic>RNA, Small Interfering - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Yunhui</creatorcontrib><creatorcontrib>Cheng, Xin</creatorcontrib><creatorcontrib>Li, Shuangjing</creatorcontrib><creatorcontrib>Zhou, Yuan</creatorcontrib><creatorcontrib>Wang, Jianxiang</creatorcontrib><creatorcontrib>Cheng, Tao</creatorcontrib><creatorcontrib>Yang, Ming</creatorcontrib><creatorcontrib>Xiong, Dongsheng</creatorcontrib><collection>Pascal-Francis</collection><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>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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 Central UK/Ireland</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>Cancer chemotherapy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Yunhui</au><au>Cheng, Xin</au><au>Li, Shuangjing</au><au>Zhou, Yuan</au><au>Wang, Jianxiang</au><au>Cheng, Tao</au><au>Yang, Ming</au><au>Xiong, Dongsheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of sorcin reverses multidrug resistance of K562/A02 cells and MCF-7/A02 cells via regulating apoptosis-related proteins</atitle><jtitle>Cancer chemotherapy and pharmacology</jtitle><stitle>Cancer Chemother Pharmacol</stitle><addtitle>Cancer Chemother Pharmacol</addtitle><date>2013-10-01</date><risdate>2013</risdate><volume>72</volume><issue>4</issue><spage>789</spage><epage>798</epage><pages>789-798</pages><issn>0344-5704</issn><eissn>1432-0843</eissn><coden>CCPHDZ</coden><abstract>Purpose
Sorcin, a 22-kDa calcium-binding protein, renders cancer cells resistant to chemotherapeutic agents, thus playing an important role in multidrug resistance (MDR). But the mechanisms mediated by sorcin still remain quite elusive. This study aim to explore whether sorcin silencing could restore chemosensitivity in MDR cancer cells and seek to identify the functional mechanisms mediated by sorcin.
Methods
To investigate the mechanisms of sorcin-silencing-induced chemosensitivity, transient expression of sorcin-siRNAs was performed in doxorubicin-induced MDR cell lines, K562/A02 and MCF-7/A02. Sensitivity to five chemotherapeutic agents was evaluated by analysis of cell survival and cell apoptosis.
Results
In this report, we show that down-regulation of sorcin did not alter expression or function of P-gp, but actually induced cell apoptosis and chemosensitivity in K562/A02 and MCF-7/A02. We also observe that silencing of sorcin-enhanced chemotherapeutic agent effects partly through regulating apoptosis-related protein, including Bcl-2, Bax, c-jun and c-fos.
Conclusion
This offers the rationale for the development of therapeutic strategies down-regulating sorcin expression for the treatment of cancer, especially for the reversal of MDR.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>24013575</pmid><doi>10.1007/s00280-013-2254-2</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0344-5704 |
| ispartof | Cancer chemotherapy and pharmacology, 2013-10, Vol.72 (4), p.789-798 |
| issn | 0344-5704 1432-0843 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1437578226 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Antineoplastic agents Antineoplastic Agents - pharmacology Apoptosis - drug effects ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism Biological and medical sciences Breast Neoplasms - drug therapy Calcium-Binding Proteins - genetics Cancer Research Cell Survival - drug effects Down-Regulation Doxorubicin - pharmacology Drug Resistance, Multiple Drug Resistance, Neoplasm - genetics Female Gene Silencing Humans K562 Cells Leukemia - drug therapy MCF-7 Cells Medical sciences Medicine Medicine & Public Health Oncology Original Article Pharmacology. Drug treatments Pharmacology/Toxicology RNA, Small Interfering - administration & dosage |
| title | Inhibition of sorcin reverses multidrug resistance of K562/A02 cells and MCF-7/A02 cells via regulating apoptosis-related proteins |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T22%3A58%3A59IST&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%20sorcin%20reverses%20multidrug%20resistance%20of%20K562/A02%20cells%20and%20MCF-7/A02%20cells%20via%20regulating%20apoptosis-related%20proteins&rft.jtitle=Cancer%20chemotherapy%20and%20pharmacology&rft.au=Hu,%20Yunhui&rft.date=2013-10-01&rft.volume=72&rft.issue=4&rft.spage=789&rft.epage=798&rft.pages=789-798&rft.issn=0344-5704&rft.eissn=1432-0843&rft.coden=CCPHDZ&rft_id=info:doi/10.1007/s00280-013-2254-2&rft_dat=%3Cproquest_cross%3E3082013541%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=1436662157&rft_id=info:pmid/24013575&rfr_iscdi=true |