Study on the Association Between miRNA-202 Expression and Drug Sensitivity in Multiple Myeloma Cells
An increasing amount of experimental evidence has shown that miRNAs play a causal role in hematologic tumorigenesis. In this study, we characterized the role of miR-202 in multiple myeloma (MM) drug sensitivity. The potential binding site of miR-202 and B cell-activating factor (BAFF) was confirmed...
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| Veröffentlicht in: | Pathology oncology research 2016-07, Vol.22 (3), p.531-539 |
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| creator | Shen, Xianjuan Guo, Yuehua Qi, Jing Shi, Wei Wu, Xinhua Ni, Hongbing Ju, Shaoqing |
| description | An increasing amount of experimental evidence has shown that miRNAs play a causal role in hematologic tumorigenesis. In this study, we characterized the role of miR-202 in multiple myeloma (MM) drug sensitivity. The potential binding site of miR-202 and B cell-activating factor (BAFF) was confirmed by luciferase reporter assay. MM cells were transfected with miR-202 mimics and inhibitor. Cells growth was measured by WST-1 cell proliferation assay and Annexin V-FLUOS apoptosis assay. BAFF and miR-202 mRNA levels were measured by real-time PCR. Meanwhile, BAFF, Bcl-2 family survival proteins and MAPK pathway proteins were measured by Western blot. It was found that miR-202 was functioned as a modulator of BAFF expression. miR-202 over-expression sensitized MM cells to bortezomib (Bort) but less to Thalidomide (Thal) and dexamethasone (Dex). miR-202 mimics in combination with Bort inhibited MM cell survival more effectively as compared with Bort treatment alone. Our study also provided experimental evidence that JNK/SAPK signaling pathway was involved in the regulatory effect of miR-202 on drug resistance of MM cells. These results suggest that the regulatory mechanism of miR-202 expression may be a promising target for fine-tuning anti-myeloma therapy. |
| doi_str_mv | 10.1007/s12253-015-0035-4 |
| format | Article |
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In this study, we characterized the role of miR-202 in multiple myeloma (MM) drug sensitivity. The potential binding site of miR-202 and B cell-activating factor (BAFF) was confirmed by luciferase reporter assay. MM cells were transfected with miR-202 mimics and inhibitor. Cells growth was measured by WST-1 cell proliferation assay and Annexin V-FLUOS apoptosis assay. BAFF and miR-202 mRNA levels were measured by real-time PCR. Meanwhile, BAFF, Bcl-2 family survival proteins and MAPK pathway proteins were measured by Western blot. It was found that miR-202 was functioned as a modulator of BAFF expression. miR-202 over-expression sensitized MM cells to bortezomib (Bort) but less to Thalidomide (Thal) and dexamethasone (Dex). miR-202 mimics in combination with Bort inhibited MM cell survival more effectively as compared with Bort treatment alone. Our study also provided experimental evidence that JNK/SAPK signaling pathway was involved in the regulatory effect of miR-202 on drug resistance of MM cells. These results suggest that the regulatory mechanism of miR-202 expression may be a promising target for fine-tuning anti-myeloma therapy.</description><identifier>ISSN: 1219-4956</identifier><identifier>EISSN: 1532-2807</identifier><identifier>DOI: 10.1007/s12253-015-0035-4</identifier><identifier>PMID: 26689580</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Aged ; Apoptosis - genetics ; Apoptosis Regulatory Proteins - genetics ; B-Cell Activating Factor - genetics ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Line, Tumor ; Cell Proliferation - genetics ; Dexamethasone - pharmacology ; Drug Resistance, Neoplasm - genetics ; Female ; Gene Expression Regulation, Neoplastic - genetics ; Humans ; Immunology ; Male ; MAP Kinase Kinase 4 - genetics ; MicroRNAs - genetics ; Middle Aged ; Mitogen-Activated Protein Kinases - genetics ; Multiple Myeloma - drug therapy ; Multiple Myeloma - genetics ; Oncology ; Original Article ; Pathology ; Proto-Oncogene Proteins c-bcl-2 - genetics ; RNA, Messenger - genetics ; Signal Transduction ; Thalidomide - pharmacology</subject><ispartof>Pathology oncology research, 2016-07, Vol.22 (3), p.531-539</ispartof><rights>Arányi Lajos Foundation 2015</rights><rights>Arányi Lajos Foundation 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-a994d497a94f526b7a67eac9d7be4c81de9b341322dd58ad7eb68b49fc8fb1e63</citedby><cites>FETCH-LOGICAL-c372t-a994d497a94f526b7a67eac9d7be4c81de9b341322dd58ad7eb68b49fc8fb1e63</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/s12253-015-0035-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12253-015-0035-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26689580$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shen, Xianjuan</creatorcontrib><creatorcontrib>Guo, Yuehua</creatorcontrib><creatorcontrib>Qi, Jing</creatorcontrib><creatorcontrib>Shi, Wei</creatorcontrib><creatorcontrib>Wu, Xinhua</creatorcontrib><creatorcontrib>Ni, Hongbing</creatorcontrib><creatorcontrib>Ju, Shaoqing</creatorcontrib><title>Study on the Association Between miRNA-202 Expression and Drug Sensitivity in Multiple Myeloma Cells</title><title>Pathology oncology research</title><addtitle>Pathol. Oncol. Res</addtitle><addtitle>Pathol Oncol Res</addtitle><description>An increasing amount of experimental evidence has shown that miRNAs play a causal role in hematologic tumorigenesis. In this study, we characterized the role of miR-202 in multiple myeloma (MM) drug sensitivity. The potential binding site of miR-202 and B cell-activating factor (BAFF) was confirmed by luciferase reporter assay. MM cells were transfected with miR-202 mimics and inhibitor. Cells growth was measured by WST-1 cell proliferation assay and Annexin V-FLUOS apoptosis assay. BAFF and miR-202 mRNA levels were measured by real-time PCR. Meanwhile, BAFF, Bcl-2 family survival proteins and MAPK pathway proteins were measured by Western blot. It was found that miR-202 was functioned as a modulator of BAFF expression. miR-202 over-expression sensitized MM cells to bortezomib (Bort) but less to Thalidomide (Thal) and dexamethasone (Dex). miR-202 mimics in combination with Bort inhibited MM cell survival more effectively as compared with Bort treatment alone. Our study also provided experimental evidence that JNK/SAPK signaling pathway was involved in the regulatory effect of miR-202 on drug resistance of MM cells. These results suggest that the regulatory mechanism of miR-202 expression may be a promising target for fine-tuning anti-myeloma therapy.</description><subject>Aged</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>B-Cell Activating Factor - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Dexamethasone - pharmacology</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Humans</subject><subject>Immunology</subject><subject>Male</subject><subject>MAP Kinase Kinase 4 - genetics</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>Mitogen-Activated Protein Kinases - genetics</subject><subject>Multiple Myeloma - drug therapy</subject><subject>Multiple Myeloma - genetics</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>Signal Transduction</subject><subject>Thalidomide - pharmacology</subject><issn>1219-4956</issn><issn>1532-2807</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kUlvFDEQhS1ERJKBH8AFWeLCxYnt9tI-DpNVyiKR5Gy529XBUS-D7Q6Zf49HExBC4uSy6nuvSvUQ-sjoEaNUHyfGuawIZZJQWkki3qADJitOeE3121JzZogwUu2jw5SeaNEoo96hfa5UbWRND5C_y7Pf4GnE-TvgZUpTG1wO5f8V8k-AEQ_h282ScMrx6cs6Qkrbphs9PonzI76DMYUcnkPe4DDi67nPYd0Dvt5APw0Or6Dv03u017k-wYfXd4Eezk7vVxfk6vb8crW8Im2leSbOGOGF0c6ITnLVaKc0uNZ43YBoa-bBNJVgFefey9p5DY2qG2G6tu4aBqpaoC8733WcfsyQsh1CassGboRpTpZpU0mlBNMF_fwP-jTNcSzbbSmuaW0KvEBsR7VxSilCZ9cxDC5uLKN2G4HdRWBLBHYbgRVF8-nVeW4G8H8Uv29eAL4DUmmNjxD_Gv1f11_K6JDA</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Shen, Xianjuan</creator><creator>Guo, Yuehua</creator><creator>Qi, Jing</creator><creator>Shi, Wei</creator><creator>Wu, Xinhua</creator><creator>Ni, Hongbing</creator><creator>Ju, Shaoqing</creator><general>Springer Netherlands</general><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160701</creationdate><title>Study on the Association Between miRNA-202 Expression and Drug Sensitivity in Multiple Myeloma Cells</title><author>Shen, Xianjuan ; 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Oncol. Res</stitle><addtitle>Pathol Oncol Res</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>22</volume><issue>3</issue><spage>531</spage><epage>539</epage><pages>531-539</pages><issn>1219-4956</issn><eissn>1532-2807</eissn><abstract>An increasing amount of experimental evidence has shown that miRNAs play a causal role in hematologic tumorigenesis. In this study, we characterized the role of miR-202 in multiple myeloma (MM) drug sensitivity. The potential binding site of miR-202 and B cell-activating factor (BAFF) was confirmed by luciferase reporter assay. MM cells were transfected with miR-202 mimics and inhibitor. Cells growth was measured by WST-1 cell proliferation assay and Annexin V-FLUOS apoptosis assay. BAFF and miR-202 mRNA levels were measured by real-time PCR. Meanwhile, BAFF, Bcl-2 family survival proteins and MAPK pathway proteins were measured by Western blot. It was found that miR-202 was functioned as a modulator of BAFF expression. miR-202 over-expression sensitized MM cells to bortezomib (Bort) but less to Thalidomide (Thal) and dexamethasone (Dex). miR-202 mimics in combination with Bort inhibited MM cell survival more effectively as compared with Bort treatment alone. Our study also provided experimental evidence that JNK/SAPK signaling pathway was involved in the regulatory effect of miR-202 on drug resistance of MM cells. These results suggest that the regulatory mechanism of miR-202 expression may be a promising target for fine-tuning anti-myeloma therapy.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>26689580</pmid><doi>10.1007/s12253-015-0035-4</doi><tpages>9</tpages></addata></record> |
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| subjects | Aged Apoptosis - genetics Apoptosis Regulatory Proteins - genetics B-Cell Activating Factor - genetics Biomedical and Life Sciences Biomedicine Cancer Research Cell Line, Tumor Cell Proliferation - genetics Dexamethasone - pharmacology Drug Resistance, Neoplasm - genetics Female Gene Expression Regulation, Neoplastic - genetics Humans Immunology Male MAP Kinase Kinase 4 - genetics MicroRNAs - genetics Middle Aged Mitogen-Activated Protein Kinases - genetics Multiple Myeloma - drug therapy Multiple Myeloma - genetics Oncology Original Article Pathology Proto-Oncogene Proteins c-bcl-2 - genetics RNA, Messenger - genetics Signal Transduction Thalidomide - pharmacology |
| title | Study on the Association Between miRNA-202 Expression and Drug Sensitivity in Multiple Myeloma Cells |
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