miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer
It is not well established whether miR-93 is involved in drug resistance and epithelial-mesenchymal transition (EMT) in breast cancer, and its underlying mechanism remains uncertain. In the present study, the expression differences of miR-93 between paired breast cancer tissues confirmed it is invol...
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| Veröffentlicht in: | Oncology reports 2017-10, Vol.38 (4), p.2401-2407 |
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| creator | Chu, Shihua Liu, Geng Xia, Peixuan Chen, Guoqing Shi, Feng Yi, Tao Zhou, Hongying |
| description | It is not well established whether miR-93 is involved in drug resistance and epithelial-mesenchymal transition (EMT) in breast cancer, and its underlying mechanism remains uncertain. In the present study, the expression differences of miR-93 between paired breast cancer tissues confirmed it is involved in the progression of breast cancer. Such a difference was also observed in doxorubicin-resistant and -sensitive cells. Overexpressed miR-93 in sensitive cells revealed increases in cellular proliferation and the expression levels of drug-resistant-related genes, and a decrease in sensitivity to doxorubicin. This demonstrated the relationship between miR-93 and breast cancer drug resistance. Simultaneously, EMT was confirmed in miR-93 overexpressing sensitive cells. This indicated the triadic relationship among miR-93, EMT and drug resistance in breast cancer. We applied the Dual-luciferase Reporter assay to expose the direct interaction between miR-93 and PTEN, which suggested that miR-93 contributes to inducing EMT and drug resistance of breast cancer cells by targeting PTEN. |
| doi_str_mv | 10.3892/or.2017.5859 |
| format | Article |
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In the present study, the expression differences of miR-93 between paired breast cancer tissues confirmed it is involved in the progression of breast cancer. Such a difference was also observed in doxorubicin-resistant and -sensitive cells. Overexpressed miR-93 in sensitive cells revealed increases in cellular proliferation and the expression levels of drug-resistant-related genes, and a decrease in sensitivity to doxorubicin. This demonstrated the relationship between miR-93 and breast cancer drug resistance. Simultaneously, EMT was confirmed in miR-93 overexpressing sensitive cells. This indicated the triadic relationship among miR-93, EMT and drug resistance in breast cancer. We applied the Dual-luciferase Reporter assay to expose the direct interaction between miR-93 and PTEN, which suggested that miR-93 contributes to inducing EMT and drug resistance of breast cancer cells by targeting PTEN.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2017.5859</identifier><identifier>PMID: 28765915</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Apoptosis ; Bioinformatics ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cell Proliferation - genetics ; Doxorubicin - administration & dosage ; Doxorubicin - adverse effects ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Epithelial-Mesenchymal Transition - genetics ; Ethics ; Female ; Gene Expression Regulation, Neoplastic ; Genes ; Humans ; MCF-7 Cells ; Medical prognosis ; MicroRNAs - genetics ; PTEN Phosphohydrolase - genetics ; Software ; Statistical analysis ; Studies</subject><ispartof>Oncology reports, 2017-10, Vol.38 (4), p.2401-2407</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-f270148c70fa95a9aef2af3dc3d20621f034616811d440b86338bdf9b5f990bb3</citedby><cites>FETCH-LOGICAL-c423t-f270148c70fa95a9aef2af3dc3d20621f034616811d440b86338bdf9b5f990bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28765915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chu, Shihua</creatorcontrib><creatorcontrib>Liu, Geng</creatorcontrib><creatorcontrib>Xia, Peixuan</creatorcontrib><creatorcontrib>Chen, Guoqing</creatorcontrib><creatorcontrib>Shi, Feng</creatorcontrib><creatorcontrib>Yi, Tao</creatorcontrib><creatorcontrib>Zhou, Hongying</creatorcontrib><title>miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>It is not well established whether miR-93 is involved in drug resistance and epithelial-mesenchymal transition (EMT) in breast cancer, and its underlying mechanism remains uncertain. 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We applied the Dual-luciferase Reporter assay to expose the direct interaction between miR-93 and PTEN, which suggested that miR-93 contributes to inducing EMT and drug resistance of breast cancer cells by targeting PTEN.</description><subject>Apoptosis</subject><subject>Bioinformatics</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Proliferation - genetics</subject><subject>Doxorubicin - administration & dosage</subject><subject>Doxorubicin - adverse effects</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Ethics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Humans</subject><subject>MCF-7 Cells</subject><subject>Medical prognosis</subject><subject>MicroRNAs - genetics</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>Software</subject><subject>Statistical analysis</subject><subject>Studies</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkEtLAzEURoMotlZ3riXgxoVT85yZuJNSH1gflAruQpJJZMp0UpMZsP_eGVtduLqXy7kfHweAU4zGNBfkyocxQTgb85yLPTDEmcAJYRTvdzsiOKGUvw_AUYxLhEiGUnEIBiTPUi4wH4L5qpwngkJVF_B1MX2-ho92A4P9aCvV-BChd7DwXz60ujRlnQQby9io2tifl-nTApY11MGq2EDT38MxOHCqivZkN0fg7Xa6mNwns5e7h8nNLDGM0CZxXRnMcpMhpwRXQllHlKOFoQVBKcEOUZbiNMe4YAzpPKU014UTmjshkNZ0BC62uevgP1sbG7kqo7FVpWrr2yixIJxjnGasQ8__oUvfhrpr11GdMEKZyDvqckuZ4GMM1sl1KFcqbCRGsnctfZC9a9m77vCzXWirV7b4g3_l0m8T-XdG</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Chu, Shihua</creator><creator>Liu, Geng</creator><creator>Xia, Peixuan</creator><creator>Chen, Guoqing</creator><creator>Shi, Feng</creator><creator>Yi, Tao</creator><creator>Zhou, Hongying</creator><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</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>20171001</creationdate><title>miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer</title><author>Chu, Shihua ; 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In the present study, the expression differences of miR-93 between paired breast cancer tissues confirmed it is involved in the progression of breast cancer. Such a difference was also observed in doxorubicin-resistant and -sensitive cells. Overexpressed miR-93 in sensitive cells revealed increases in cellular proliferation and the expression levels of drug-resistant-related genes, and a decrease in sensitivity to doxorubicin. This demonstrated the relationship between miR-93 and breast cancer drug resistance. Simultaneously, EMT was confirmed in miR-93 overexpressing sensitive cells. This indicated the triadic relationship among miR-93, EMT and drug resistance in breast cancer. 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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Apoptosis Bioinformatics Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - pathology Cell Proliferation - genetics Doxorubicin - administration & dosage Doxorubicin - adverse effects Drug resistance Drug Resistance, Neoplasm - genetics Epithelial-Mesenchymal Transition - genetics Ethics Female Gene Expression Regulation, Neoplastic Genes Humans MCF-7 Cells Medical prognosis MicroRNAs - genetics PTEN Phosphohydrolase - genetics Software Statistical analysis Studies |
| title | miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer |
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