STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells
Signal transducer and activator of transcription 3 (STAT3) controls cell survival, growth, migration, and invasion. Here, we observed that STAT3 exerted anti-apoptotic effects in breast cancer cells. On the other hand, miR-17-5p induced apoptosis in breast cancer cells, and overexpression of miR-17-...
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| Veröffentlicht in: | Oncotarget 2017-02, Vol.8 (9), p.15763-15774 |
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| creator | Liao, Xing-Hua Xiang, Yuan Yu, Cheng-Xi Li, Jia-Peng Li, Hui Nie, Qi Hu, Peng Zhou, Jun Zhang, Tong-Cun |
| description | Signal transducer and activator of transcription 3 (STAT3) controls cell survival, growth, migration, and invasion. Here, we observed that STAT3 exerted anti-apoptotic effects in breast cancer cells. On the other hand, miR-17-5p induced apoptosis in breast cancer cells, and overexpression of miR-17-5p sensitized MCF-7 cells to paclitaxel-induced apoptosis via STAT3. Overexpression of STAT3 in MCF-7 cells decreased paclitaxel-induced apoptosis, but STAT3 knockout abolished the miR-17-5p-induced increases in apoptosis. Finally, miR-17-5p promoted apoptosis by increasing p53 expression, which was inhibited by STAT3. These results demonstrate a novel pathway via which miR-17-5p inhibits STAT3 and increases p53 expression to promote apoptosis in breast cancer cells. |
| doi_str_mv | 10.18632/oncotarget.15000 |
| format | Article |
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Here, we observed that STAT3 exerted anti-apoptotic effects in breast cancer cells. On the other hand, miR-17-5p induced apoptosis in breast cancer cells, and overexpression of miR-17-5p sensitized MCF-7 cells to paclitaxel-induced apoptosis via STAT3. Overexpression of STAT3 in MCF-7 cells decreased paclitaxel-induced apoptosis, but STAT3 knockout abolished the miR-17-5p-induced increases in apoptosis. Finally, miR-17-5p promoted apoptosis by increasing p53 expression, which was inhibited by STAT3. These results demonstrate a novel pathway via which miR-17-5p inhibits STAT3 and increases p53 expression to promote apoptosis in breast cancer cells.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.15000</identifier><identifier>PMID: 28178652</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>3' Untranslated Regions - genetics ; Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis - drug effects ; Apoptosis - genetics ; Blotting, Western ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Line, Tumor ; Cell Survival - drug effects ; Cell Survival - genetics ; Estrogen Antagonists - pharmacology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; MCF-7 Cells ; MicroRNAs - genetics ; Paclitaxel - pharmacology ; Research Paper ; Reverse Transcriptase Polymerase Chain Reaction ; STAT3 Transcription Factor - genetics ; STAT3 Transcription Factor - metabolism ; Tamoxifen - pharmacology ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Oncotarget, 2017-02, Vol.8 (9), p.15763-15774</ispartof><rights>Copyright: © 2017 Liao et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-d1230c8d176b645420ea82d049edf21b8d464ffc1ae5e266caeeee140fba8fa93</citedby><cites>FETCH-LOGICAL-c422t-d1230c8d176b645420ea82d049edf21b8d464ffc1ae5e266caeeee140fba8fa93</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/PMC5362521/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5362521/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28178652$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liao, Xing-Hua</creatorcontrib><creatorcontrib>Xiang, Yuan</creatorcontrib><creatorcontrib>Yu, Cheng-Xi</creatorcontrib><creatorcontrib>Li, Jia-Peng</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Nie, Qi</creatorcontrib><creatorcontrib>Hu, Peng</creatorcontrib><creatorcontrib>Zhou, Jun</creatorcontrib><creatorcontrib>Zhang, Tong-Cun</creatorcontrib><title>STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Signal transducer and activator of transcription 3 (STAT3) controls cell survival, growth, migration, and invasion. Here, we observed that STAT3 exerted anti-apoptotic effects in breast cancer cells. On the other hand, miR-17-5p induced apoptosis in breast cancer cells, and overexpression of miR-17-5p sensitized MCF-7 cells to paclitaxel-induced apoptosis via STAT3. Overexpression of STAT3 in MCF-7 cells decreased paclitaxel-induced apoptosis, but STAT3 knockout abolished the miR-17-5p-induced increases in apoptosis. Finally, miR-17-5p promoted apoptosis by increasing p53 expression, which was inhibited by STAT3. These results demonstrate a novel pathway via which miR-17-5p inhibits STAT3 and increases p53 expression to promote apoptosis in breast cancer cells.</description><subject>3' Untranslated Regions - genetics</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - genetics</subject><subject>Estrogen Antagonists - pharmacology</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>MCF-7 Cells</subject><subject>MicroRNAs - genetics</subject><subject>Paclitaxel - pharmacology</subject><subject>Research Paper</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Tamoxifen - pharmacology</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU1v3CAQhlHVKhtt8wNyqTj24gQwsPYlUhQ1H1KqSs3mjMZ4vEu0Cw7gSMmvD5uvplxAwzvvO6OHkEPOjnija3EcvA0Z4grzEVeMsS9kn7eyrYRS9ddP7xk5SOmuCJiSi0a0e2QmGr5otBL7JNwsT5c1dYlGvJ9cxJ4OIdLf7m_FF5Uaqy32DnIpJ_TJZfcE2QVPc6B2jduQ1xhhfKyc7ydbVDCGMYdU_JynXURImVrwFiO1uNmk7-TbAJuEB2_3nNye_1qeXVbXfy6uzk6vKyuFyFXPRc1s0_OF7rRUUjCERvRMttgPgndNL7UcBssBFQqtLWA5XLKhg2aAtp6Tk1ffcerKChZ9jrAxY3RbiI8mgDP__3i3NqvwYFSthRK8GPx8M4jhfsKUzdal3QrgMUzJFAZat4KpXRZ_ldoYUoo4fMRwZl5YmX-szAur0vPj83wfHe9k6mfra5Vt</recordid><startdate>20170228</startdate><enddate>20170228</enddate><creator>Liao, Xing-Hua</creator><creator>Xiang, Yuan</creator><creator>Yu, Cheng-Xi</creator><creator>Li, Jia-Peng</creator><creator>Li, Hui</creator><creator>Nie, Qi</creator><creator>Hu, Peng</creator><creator>Zhou, Jun</creator><creator>Zhang, Tong-Cun</creator><general>Impact Journals LLC</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>20170228</creationdate><title>STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells</title><author>Liao, Xing-Hua ; Xiang, Yuan ; Yu, Cheng-Xi ; Li, Jia-Peng ; Li, Hui ; Nie, Qi ; Hu, Peng ; Zhou, Jun ; Zhang, Tong-Cun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-d1230c8d176b645420ea82d049edf21b8d464ffc1ae5e266caeeee140fba8fa93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>3' Untranslated Regions - genetics</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - genetics</topic><topic>Estrogen Antagonists - pharmacology</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>MCF-7 Cells</topic><topic>MicroRNAs - genetics</topic><topic>Paclitaxel - pharmacology</topic><topic>Research Paper</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Tamoxifen - pharmacology</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Liao, Xing-Hua</creatorcontrib><creatorcontrib>Xiang, Yuan</creatorcontrib><creatorcontrib>Yu, Cheng-Xi</creatorcontrib><creatorcontrib>Li, Jia-Peng</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Nie, Qi</creatorcontrib><creatorcontrib>Hu, Peng</creatorcontrib><creatorcontrib>Zhou, Jun</creatorcontrib><creatorcontrib>Zhang, Tong-Cun</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>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liao, Xing-Hua</au><au>Xiang, Yuan</au><au>Yu, Cheng-Xi</au><au>Li, Jia-Peng</au><au>Li, Hui</au><au>Nie, Qi</au><au>Hu, Peng</au><au>Zhou, Jun</au><au>Zhang, Tong-Cun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2017-02-28</date><risdate>2017</risdate><volume>8</volume><issue>9</issue><spage>15763</spage><epage>15774</epage><pages>15763-15774</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Signal transducer and activator of transcription 3 (STAT3) controls cell survival, growth, migration, and invasion. Here, we observed that STAT3 exerted anti-apoptotic effects in breast cancer cells. On the other hand, miR-17-5p induced apoptosis in breast cancer cells, and overexpression of miR-17-5p sensitized MCF-7 cells to paclitaxel-induced apoptosis via STAT3. Overexpression of STAT3 in MCF-7 cells decreased paclitaxel-induced apoptosis, but STAT3 knockout abolished the miR-17-5p-induced increases in apoptosis. Finally, miR-17-5p promoted apoptosis by increasing p53 expression, which was inhibited by STAT3. These results demonstrate a novel pathway via which miR-17-5p inhibits STAT3 and increases p53 expression to promote apoptosis in breast cancer cells.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>28178652</pmid><doi>10.18632/oncotarget.15000</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated Regions - genetics Antineoplastic Agents, Phytogenic - pharmacology Apoptosis - drug effects Apoptosis - genetics Blotting, Western Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Line, Tumor Cell Survival - drug effects Cell Survival - genetics Estrogen Antagonists - pharmacology Female Gene Expression Regulation, Neoplastic Humans MCF-7 Cells MicroRNAs - genetics Paclitaxel - pharmacology Research Paper Reverse Transcriptase Polymerase Chain Reaction STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Tamoxifen - pharmacology Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| title | STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells |
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