Upregulation of the inwardly rectifying potassium channel Kir2.1 (KCNJ2) modulates multidrug resistance of small-cell lung cancer under the regulation of miR-7 and the Ras/MAPK pathway
KCNJ2/Kir2.1, a member of the classical inwardly rectifying potassium channel family, is commonly expressed in a wide range of tissues and cell types. Previous studies indicated that Kir2.1 may be associated with SCLC multidrug resistance (MDR). However, whether Kir2.1 can regulate MDR and its under...
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| Veröffentlicht in: | Molecular cancer 2015-03, Vol.14 (1), p.59-59, Article 59 |
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| creator | Liu, Huanxin Huang, Jie Peng, Juan Wu, Xiaoxia Zhang, Yan Zhu, Weiliang Guo, Linlang |
| description | KCNJ2/Kir2.1, a member of the classical inwardly rectifying potassium channel family, is commonly expressed in a wide range of tissues and cell types. Previous studies indicated that Kir2.1 may be associated with SCLC multidrug resistance (MDR). However, whether Kir2.1 can regulate MDR and its underlying mechanisms remain poorly understood in SCLC.
KCNJ2/Kir2.1 expression was examined in tissues from fifty-two SCLC cases by immunohistochemistry. Overexpression or knockdown of KCNJ2/Kir21 was performed in multidrug-resistant SCLC cell lines (H69AR and H446AR) and their parental cell lines (H69 and H446) to assess its influence on cell growth, apoptosis, the cell cycle and chemoresistance.
KCNJ2/Kir2.1 was expressed in 44.23% (23/52) of SCLC tissues. Overexpression of KCNJ2/Kir2.1 was correlated with the clinical stage and chemotherapy response in SCLC patients. Knockdown of KCNJ2/Kir2.1 expression using KCNJ2/Kir2.1 shRNA in H69AR and H446AR cells inhibited cell growth and sensitized the cancer cells to chemotherapeutic drugs by increasing cell apoptosis and cell cycle arrest. Forced KCNJ2/Kir2.1 expression in H69 and H446 cells promoted cell growth and enhanced multidrug resistance via reduced drug-induced apoptosis accompanied by cell cycle arrest. KCNJ2/Kir2.1 expression was also influenced by PKC and MEK inhibitors. In addition, multidrug resistance protein 1 (MRP1/ABCC1) was confirmed to interact with KCNJ2/Kir2.1 by Co-IP assays.
KCNJ2/Kir2.1 modulates cell growth and drug resistance by regulating MRP1/ABCC1 expression and is simultaneously regulated by the Ras/MAPK pathway and miR-7. KCNJ2/Kir2.1 may be a prognostic predictor and a potentially novel target for interfering with chemoresistance in SCLC. |
| doi_str_mv | 10.1186/s12943-015-0298-0 |
| format | Article |
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KCNJ2/Kir2.1 expression was examined in tissues from fifty-two SCLC cases by immunohistochemistry. Overexpression or knockdown of KCNJ2/Kir21 was performed in multidrug-resistant SCLC cell lines (H69AR and H446AR) and their parental cell lines (H69 and H446) to assess its influence on cell growth, apoptosis, the cell cycle and chemoresistance.
KCNJ2/Kir2.1 was expressed in 44.23% (23/52) of SCLC tissues. Overexpression of KCNJ2/Kir2.1 was correlated with the clinical stage and chemotherapy response in SCLC patients. Knockdown of KCNJ2/Kir2.1 expression using KCNJ2/Kir2.1 shRNA in H69AR and H446AR cells inhibited cell growth and sensitized the cancer cells to chemotherapeutic drugs by increasing cell apoptosis and cell cycle arrest. Forced KCNJ2/Kir2.1 expression in H69 and H446 cells promoted cell growth and enhanced multidrug resistance via reduced drug-induced apoptosis accompanied by cell cycle arrest. KCNJ2/Kir2.1 expression was also influenced by PKC and MEK inhibitors. In addition, multidrug resistance protein 1 (MRP1/ABCC1) was confirmed to interact with KCNJ2/Kir2.1 by Co-IP assays.
KCNJ2/Kir2.1 modulates cell growth and drug resistance by regulating MRP1/ABCC1 expression and is simultaneously regulated by the Ras/MAPK pathway and miR-7. KCNJ2/Kir2.1 may be a prognostic predictor and a potentially novel target for interfering with chemoresistance in SCLC.</description><identifier>ISSN: 1476-4598</identifier><identifier>EISSN: 1476-4598</identifier><identifier>DOI: 10.1186/s12943-015-0298-0</identifier><identifier>PMID: 25880778</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adult ; Aged ; Analysis ; Animals ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Apoptosis - drug effects ; Apoptosis - genetics ; Cancer ; Cell Cycle Checkpoints - drug effects ; Cell Cycle Checkpoints - genetics ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chemotherapy ; Disease Models, Animal ; Drug Resistance, Multiple - genetics ; Drug Resistance, Neoplasm - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Health aspects ; Humans ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - mortality ; Lung Neoplasms - pathology ; Male ; MicroRNAs - genetics ; Middle Aged ; Mitogen-Activated Protein Kinases ; Multidrug Resistance-Associated Proteins - metabolism ; Neoplasm Staging ; Potassium Channels, Inwardly Rectifying - genetics ; Potassium Channels, Inwardly Rectifying - metabolism ; Prognosis ; Protein Binding ; Proto-Oncogene Proteins p21(ras) ; Risk Factors ; RNA Interference ; Signal Transduction ; Small Cell Lung Carcinoma - drug therapy ; Small Cell Lung Carcinoma - genetics ; Small Cell Lung Carcinoma - metabolism ; Small Cell Lung Carcinoma - mortality ; Small Cell Lung Carcinoma - pathology ; Tumor Burden - drug effects ; Xenograft Model Antitumor Assays</subject><ispartof>Molecular cancer, 2015-03, Vol.14 (1), p.59-59, Article 59</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Liu et al.; licensee BioMed Central. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-443c9977fc7f8942bf2b5cb225b44e6ff58ed0ca7672de4ca2682305ea4ac28e3</citedby><cites>FETCH-LOGICAL-c580t-443c9977fc7f8942bf2b5cb225b44e6ff58ed0ca7672de4ca2682305ea4ac28e3</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/PMC4373128/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4373128/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25880778$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Huanxin</creatorcontrib><creatorcontrib>Huang, Jie</creatorcontrib><creatorcontrib>Peng, Juan</creatorcontrib><creatorcontrib>Wu, Xiaoxia</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Zhu, Weiliang</creatorcontrib><creatorcontrib>Guo, Linlang</creatorcontrib><title>Upregulation of the inwardly rectifying potassium channel Kir2.1 (KCNJ2) modulates multidrug resistance of small-cell lung cancer under the regulation of miR-7 and the Ras/MAPK pathway</title><title>Molecular cancer</title><addtitle>Mol Cancer</addtitle><description>KCNJ2/Kir2.1, a member of the classical inwardly rectifying potassium channel family, is commonly expressed in a wide range of tissues and cell types. Previous studies indicated that Kir2.1 may be associated with SCLC multidrug resistance (MDR). However, whether Kir2.1 can regulate MDR and its underlying mechanisms remain poorly understood in SCLC.
KCNJ2/Kir2.1 expression was examined in tissues from fifty-two SCLC cases by immunohistochemistry. Overexpression or knockdown of KCNJ2/Kir21 was performed in multidrug-resistant SCLC cell lines (H69AR and H446AR) and their parental cell lines (H69 and H446) to assess its influence on cell growth, apoptosis, the cell cycle and chemoresistance.
KCNJ2/Kir2.1 was expressed in 44.23% (23/52) of SCLC tissues. Overexpression of KCNJ2/Kir2.1 was correlated with the clinical stage and chemotherapy response in SCLC patients. Knockdown of KCNJ2/Kir2.1 expression using KCNJ2/Kir2.1 shRNA in H69AR and H446AR cells inhibited cell growth and sensitized the cancer cells to chemotherapeutic drugs by increasing cell apoptosis and cell cycle arrest. Forced KCNJ2/Kir2.1 expression in H69 and H446 cells promoted cell growth and enhanced multidrug resistance via reduced drug-induced apoptosis accompanied by cell cycle arrest. KCNJ2/Kir2.1 expression was also influenced by PKC and MEK inhibitors. In addition, multidrug resistance protein 1 (MRP1/ABCC1) was confirmed to interact with KCNJ2/Kir2.1 by Co-IP assays.
KCNJ2/Kir2.1 modulates cell growth and drug resistance by regulating MRP1/ABCC1 expression and is simultaneously regulated by the Ras/MAPK pathway and miR-7. KCNJ2/Kir2.1 may be a prognostic predictor and a potentially novel target for interfering with chemoresistance in SCLC.</description><subject>Adult</subject><subject>Aged</subject><subject>Analysis</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Cancer</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Cycle Checkpoints - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy</subject><subject>Disease Models, Animal</subject><subject>Drug Resistance, Multiple - genetics</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - mortality</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>Mitogen-Activated Protein Kinases</subject><subject>Multidrug Resistance-Associated Proteins - metabolism</subject><subject>Neoplasm Staging</subject><subject>Potassium Channels, Inwardly Rectifying - genetics</subject><subject>Potassium Channels, Inwardly Rectifying - metabolism</subject><subject>Prognosis</subject><subject>Protein Binding</subject><subject>Proto-Oncogene Proteins p21(ras)</subject><subject>Risk Factors</subject><subject>RNA Interference</subject><subject>Signal Transduction</subject><subject>Small Cell Lung Carcinoma - drug therapy</subject><subject>Small Cell Lung Carcinoma - genetics</subject><subject>Small Cell Lung Carcinoma - metabolism</subject><subject>Small Cell Lung Carcinoma - mortality</subject><subject>Small Cell Lung Carcinoma - pathology</subject><subject>Tumor Burden - drug effects</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1476-4598</issn><issn>1476-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptks1u1DAUhSMEomXgAdggS2zKIlPbcWJngzQaQYEpP6ro2nKc6xkjx07thGrejMdrwpSqIyFLtuV7zufr5GTZa4KXhIjqPBFasyLHpMwxrUWOn2SnhPEqZ2Utnj7an2QvUvqFMeGCs-fZCS2FwJyL0-zPdR9hOzo12OBRMGjYAbL-VsXW7VEEPVizt36L-jColOzYIb1T3oNDGxvpkqCzzfrbF_oOdaGdMZBQN7rBtnHcTv5k06C8hhmdOuVcrsE55MYJqedCRKNvp3m-97iTzl7lHCnf_q1dqXT-dfVjg3o17G7V_mX2zCiX4NX9usiuP374uf6UX36_-LxeXea6FHjIGSt0XXNuNDeiZrQxtCl1Q2nZMAaVMaWAFmvFK05bYFrRStACl6CY0lRAscjeH7j92HTQavBDVE720XYq7mVQVh5XvN3JbfgtWcELQsUEOLsHxHAzQhpkZ9P8EZSHMCZJKs4orgqCJ-nbg3SrHEjrTZiIepbLVckIE6Ke_vciW_5HNY0WOquDB2On8yMDORh0DClFMA_dEyznIMlDkOQUJDkHSc6tvHn87AfHv-QUd16_xl8</recordid><startdate>20150312</startdate><enddate>20150312</enddate><creator>Liu, Huanxin</creator><creator>Huang, Jie</creator><creator>Peng, Juan</creator><creator>Wu, Xiaoxia</creator><creator>Zhang, Yan</creator><creator>Zhu, Weiliang</creator><creator>Guo, Linlang</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><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>5PM</scope></search><sort><creationdate>20150312</creationdate><title>Upregulation of the inwardly rectifying potassium channel Kir2.1 (KCNJ2) modulates multidrug resistance of small-cell lung cancer under the regulation of miR-7 and the Ras/MAPK pathway</title><author>Liu, Huanxin ; Huang, Jie ; Peng, Juan ; Wu, Xiaoxia ; Zhang, Yan ; Zhu, Weiliang ; Guo, Linlang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c580t-443c9977fc7f8942bf2b5cb225b44e6ff58ed0ca7672de4ca2682305ea4ac28e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Analysis</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Cancer</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell Cycle Checkpoints - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotherapy</topic><topic>Disease Models, Animal</topic><topic>Drug Resistance, Multiple - genetics</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - mortality</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>Mitogen-Activated Protein Kinases</topic><topic>Multidrug Resistance-Associated Proteins - metabolism</topic><topic>Neoplasm Staging</topic><topic>Potassium Channels, Inwardly Rectifying - genetics</topic><topic>Potassium Channels, Inwardly Rectifying - metabolism</topic><topic>Prognosis</topic><topic>Protein Binding</topic><topic>Proto-Oncogene Proteins p21(ras)</topic><topic>Risk Factors</topic><topic>RNA Interference</topic><topic>Signal Transduction</topic><topic>Small Cell Lung Carcinoma - drug therapy</topic><topic>Small Cell Lung Carcinoma - genetics</topic><topic>Small Cell Lung Carcinoma - metabolism</topic><topic>Small Cell Lung Carcinoma - mortality</topic><topic>Small Cell Lung Carcinoma - pathology</topic><topic>Tumor Burden - drug effects</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Huanxin</creatorcontrib><creatorcontrib>Huang, Jie</creatorcontrib><creatorcontrib>Peng, Juan</creatorcontrib><creatorcontrib>Wu, Xiaoxia</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Zhu, Weiliang</creatorcontrib><creatorcontrib>Guo, Linlang</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>PubMed Central (Full Participant titles)</collection><jtitle>Molecular cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Huanxin</au><au>Huang, Jie</au><au>Peng, Juan</au><au>Wu, Xiaoxia</au><au>Zhang, Yan</au><au>Zhu, Weiliang</au><au>Guo, Linlang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of the inwardly rectifying potassium channel Kir2.1 (KCNJ2) modulates multidrug resistance of small-cell lung cancer under the regulation of miR-7 and the Ras/MAPK pathway</atitle><jtitle>Molecular cancer</jtitle><addtitle>Mol Cancer</addtitle><date>2015-03-12</date><risdate>2015</risdate><volume>14</volume><issue>1</issue><spage>59</spage><epage>59</epage><pages>59-59</pages><artnum>59</artnum><issn>1476-4598</issn><eissn>1476-4598</eissn><abstract>KCNJ2/Kir2.1, a member of the classical inwardly rectifying potassium channel family, is commonly expressed in a wide range of tissues and cell types. Previous studies indicated that Kir2.1 may be associated with SCLC multidrug resistance (MDR). However, whether Kir2.1 can regulate MDR and its underlying mechanisms remain poorly understood in SCLC.
KCNJ2/Kir2.1 expression was examined in tissues from fifty-two SCLC cases by immunohistochemistry. Overexpression or knockdown of KCNJ2/Kir21 was performed in multidrug-resistant SCLC cell lines (H69AR and H446AR) and their parental cell lines (H69 and H446) to assess its influence on cell growth, apoptosis, the cell cycle and chemoresistance.
KCNJ2/Kir2.1 was expressed in 44.23% (23/52) of SCLC tissues. Overexpression of KCNJ2/Kir2.1 was correlated with the clinical stage and chemotherapy response in SCLC patients. Knockdown of KCNJ2/Kir2.1 expression using KCNJ2/Kir2.1 shRNA in H69AR and H446AR cells inhibited cell growth and sensitized the cancer cells to chemotherapeutic drugs by increasing cell apoptosis and cell cycle arrest. Forced KCNJ2/Kir2.1 expression in H69 and H446 cells promoted cell growth and enhanced multidrug resistance via reduced drug-induced apoptosis accompanied by cell cycle arrest. KCNJ2/Kir2.1 expression was also influenced by PKC and MEK inhibitors. In addition, multidrug resistance protein 1 (MRP1/ABCC1) was confirmed to interact with KCNJ2/Kir2.1 by Co-IP assays.
KCNJ2/Kir2.1 modulates cell growth and drug resistance by regulating MRP1/ABCC1 expression and is simultaneously regulated by the Ras/MAPK pathway and miR-7. KCNJ2/Kir2.1 may be a prognostic predictor and a potentially novel target for interfering with chemoresistance in SCLC.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25880778</pmid><doi>10.1186/s12943-015-0298-0</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Analysis Animals Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis - drug effects Apoptosis - genetics Cancer Cell Cycle Checkpoints - drug effects Cell Cycle Checkpoints - genetics Cell Line, Tumor Cell Proliferation - drug effects Chemotherapy Disease Models, Animal Drug Resistance, Multiple - genetics Drug Resistance, Neoplasm - genetics Female Gene Expression Regulation, Neoplastic Health aspects Humans Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - mortality Lung Neoplasms - pathology Male MicroRNAs - genetics Middle Aged Mitogen-Activated Protein Kinases Multidrug Resistance-Associated Proteins - metabolism Neoplasm Staging Potassium Channels, Inwardly Rectifying - genetics Potassium Channels, Inwardly Rectifying - metabolism Prognosis Protein Binding Proto-Oncogene Proteins p21(ras) Risk Factors RNA Interference Signal Transduction Small Cell Lung Carcinoma - drug therapy Small Cell Lung Carcinoma - genetics Small Cell Lung Carcinoma - metabolism Small Cell Lung Carcinoma - mortality Small Cell Lung Carcinoma - pathology Tumor Burden - drug effects Xenograft Model Antitumor Assays |
| title | Upregulation of the inwardly rectifying potassium channel Kir2.1 (KCNJ2) modulates multidrug resistance of small-cell lung cancer under the regulation of miR-7 and the Ras/MAPK pathway |
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