A miR-20a/MAPK1/c-Myc regulatory feedback loop regulates breast carcinogenesis and chemoresistance
Chemoresistance often leads to the failure of breast cancer treatment. MicroRNAs (miRNAs) play an important role in the progression and chemoresistance of cancer. However, because of the complexity of the mechanisms of chemoresistance and the specificity of miRNA regulation in different cell types,...
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| Veröffentlicht in: | Cell death and differentiation 2018-02, Vol.25 (2), p.406-420 |
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| creator | Si, Wengong Shen, Jiaying Du, Chengyong Chen, Danni Gu, Xidong Li, Chenggong Yao, Minya Pan, Jie Cheng, Junchi Jiang, Donghai Xu, Liang Bao, Chang Fu, Peifen Fan, Weimin |
| description | Chemoresistance often leads to the failure of breast cancer treatment. MicroRNAs (miRNAs) play an important role in the progression and chemoresistance of cancer. However, because of the complexity of the mechanisms of chemoresistance and the specificity of miRNA regulation in different cell types, the function of miR-20a in breast cancer chemoresistance is still unclear. Here, by using miRNA microarray and high-content screening techniques, we found that miR-20a/b were significantly downregulated in breast cancer tissues compared with normal breast tissues, and low miR-20a/b expression was correlated with poor survival in breast cancer patients. Ectopic overexpression of miR-20a sensitized breast cancer cells to a broad spectrum of chemotherapy drugs and suppress their proliferation both
in vitro
and
in vivo
. Further study demonstrated that miR-20a directly targeted the 3'untranslated region of
MAPK1
, and thus downregulated the expression of P-gp and c-Myc by inhibiting the MAPK/ERK signaling pathway, whereas c-Myc can bind to the promoter region of the miR-20a gene to promote the expression of miR-20a. Together, our study identified a novel miR-20a/MAPK1/c-Myc feedback loop that regulates breast cancer growth and chemoresistance. These findings suggest that miR-20a synergizing with anticancer drugs will be a promising treatment strategy, especially for chemoresistant patients. |
| doi_str_mv | 10.1038/cdd.2017.176 |
| format | Article |
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in vitro
and
in vivo
. Further study demonstrated that miR-20a directly targeted the 3'untranslated region of
MAPK1
, and thus downregulated the expression of P-gp and c-Myc by inhibiting the MAPK/ERK signaling pathway, whereas c-Myc can bind to the promoter region of the miR-20a gene to promote the expression of miR-20a. Together, our study identified a novel miR-20a/MAPK1/c-Myc feedback loop that regulates breast cancer growth and chemoresistance. These findings suggest that miR-20a synergizing with anticancer drugs will be a promising treatment strategy, especially for chemoresistant patients.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/cdd.2017.176</identifier><identifier>PMID: 29125598</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/1857 ; 692/420/2489/68 ; Antineoplastic Agents - pharmacology ; Antineoplastic drugs ; Antitumor agents ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; c-Myc protein ; Cancer therapies ; Carcinogenesis ; Cell Biology ; Cell Cycle Analysis ; Cell proliferation ; Cell Proliferation - drug effects ; Chemoresistance ; Chemotherapy ; DNA microarrays ; Drug Resistance, Neoplasm - drug effects ; Drug Screening Assays, Antitumor ; Feedback ; Feedback loops ; Female ; Humans ; Life Sciences ; MAP kinase ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Mitogen-Activated Protein Kinase 1 - metabolism ; Myc protein ; Oligonucleotide Array Sequence Analysis ; Original Paper ; Proto-Oncogene Proteins c-myc - metabolism ; Signal transduction ; Stem Cells ; Tumor Cells, Cultured</subject><ispartof>Cell death and differentiation, 2018-02, Vol.25 (2), p.406-420</ispartof><rights>The Author(s) 2018</rights><rights>Copyright Nature Publishing Group Feb 2018</rights><rights>Copyright © 2018 The Author(s) 2018 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-23c2b9d1f028754666618eac598951f9d65d4d8d18a4ea02afc328ae6965af213</citedby><cites>FETCH-LOGICAL-c450t-23c2b9d1f028754666618eac598951f9d65d4d8d18a4ea02afc328ae6965af213</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/PMC5762853/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762853/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29125598$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Si, Wengong</creatorcontrib><creatorcontrib>Shen, Jiaying</creatorcontrib><creatorcontrib>Du, Chengyong</creatorcontrib><creatorcontrib>Chen, Danni</creatorcontrib><creatorcontrib>Gu, Xidong</creatorcontrib><creatorcontrib>Li, Chenggong</creatorcontrib><creatorcontrib>Yao, Minya</creatorcontrib><creatorcontrib>Pan, Jie</creatorcontrib><creatorcontrib>Cheng, Junchi</creatorcontrib><creatorcontrib>Jiang, Donghai</creatorcontrib><creatorcontrib>Xu, Liang</creatorcontrib><creatorcontrib>Bao, Chang</creatorcontrib><creatorcontrib>Fu, Peifen</creatorcontrib><creatorcontrib>Fan, Weimin</creatorcontrib><title>A miR-20a/MAPK1/c-Myc regulatory feedback loop regulates breast carcinogenesis and chemoresistance</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Chemoresistance often leads to the failure of breast cancer treatment. MicroRNAs (miRNAs) play an important role in the progression and chemoresistance of cancer. However, because of the complexity of the mechanisms of chemoresistance and the specificity of miRNA regulation in different cell types, the function of miR-20a in breast cancer chemoresistance is still unclear. Here, by using miRNA microarray and high-content screening techniques, we found that miR-20a/b were significantly downregulated in breast cancer tissues compared with normal breast tissues, and low miR-20a/b expression was correlated with poor survival in breast cancer patients. Ectopic overexpression of miR-20a sensitized breast cancer cells to a broad spectrum of chemotherapy drugs and suppress their proliferation both
in vitro
and
in vivo
. Further study demonstrated that miR-20a directly targeted the 3'untranslated region of
MAPK1
, and thus downregulated the expression of P-gp and c-Myc by inhibiting the MAPK/ERK signaling pathway, whereas c-Myc can bind to the promoter region of the miR-20a gene to promote the expression of miR-20a. Together, our study identified a novel miR-20a/MAPK1/c-Myc feedback loop that regulates breast cancer growth and chemoresistance. These findings suggest that miR-20a synergizing with anticancer drugs will be a promising treatment strategy, especially for chemoresistant patients.</description><subject>631/67/1857</subject><subject>692/420/2489/68</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic drugs</subject><subject>Antitumor agents</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>c-Myc protein</subject><subject>Cancer therapies</subject><subject>Carcinogenesis</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>DNA microarrays</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>Drug Screening Assays, Antitumor</subject><subject>Feedback</subject><subject>Feedback loops</subject><subject>Female</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>MAP kinase</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Myc protein</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Original Paper</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Signal transduction</subject><subject>Stem Cells</subject><subject>Tumor Cells, Cultured</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkc1LAzEQxYMoft88y4JXt02ym2xyEUrxCxVF9Bxmk9m62m5qshX635tSFQXnkgnvx5sHj5AjRgeMFmponRtwyqoBq-QG2WVlJXNR0mIz7YWguaZltUP2YnyllMpKy22ywzXjQmi1S-pRNmsfc05heDd6uGFDm98tbRZwsphC78MyaxBdDfYtm3o__xYwZnVAiH1mIdi28xPsMLYxg85l9gVnPqy-PXQWD8hWA9OIh1_vPnm-OH8aX-W395fX49FtbktB-5wXltfasYZyVYlSpmEKwaaYWrBGOylc6ZRjCkoEyqGxBVeAUksBDWfFPjlb-84X9Qydxa4PMDXz0M4gLI2H1vxVuvbFTPyHEZXkShTJ4OTLIPj3BcbevPpF6FJmw7QSQnClqkSdrikbfIwBm58LjJpVIyY1YlaNmNRIwo9_p_qBvytIQL4GYpK6CYZfV_8z_ARLupZW</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Si, Wengong</creator><creator>Shen, Jiaying</creator><creator>Du, Chengyong</creator><creator>Chen, Danni</creator><creator>Gu, Xidong</creator><creator>Li, Chenggong</creator><creator>Yao, Minya</creator><creator>Pan, Jie</creator><creator>Cheng, Junchi</creator><creator>Jiang, Donghai</creator><creator>Xu, Liang</creator><creator>Bao, Chang</creator><creator>Fu, Peifen</creator><creator>Fan, Weimin</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20180201</creationdate><title>A miR-20a/MAPK1/c-Myc regulatory feedback loop regulates breast carcinogenesis and chemoresistance</title><author>Si, Wengong ; Shen, Jiaying ; Du, Chengyong ; Chen, Danni ; Gu, Xidong ; Li, Chenggong ; Yao, Minya ; Pan, Jie ; Cheng, Junchi ; Jiang, Donghai ; Xu, Liang ; Bao, Chang ; Fu, Peifen ; Fan, Weimin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-23c2b9d1f028754666618eac598951f9d65d4d8d18a4ea02afc328ae6965af213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>631/67/1857</topic><topic>692/420/2489/68</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic drugs</topic><topic>Antitumor agents</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>c-Myc protein</topic><topic>Cancer therapies</topic><topic>Carcinogenesis</topic><topic>Cell Biology</topic><topic>Cell Cycle Analysis</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>DNA microarrays</topic><topic>Drug Resistance, Neoplasm - drug effects</topic><topic>Drug Screening Assays, Antitumor</topic><topic>Feedback</topic><topic>Feedback loops</topic><topic>Female</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>MAP kinase</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Myc protein</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Original Paper</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>Signal transduction</topic><topic>Stem Cells</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Si, Wengong</creatorcontrib><creatorcontrib>Shen, Jiaying</creatorcontrib><creatorcontrib>Du, Chengyong</creatorcontrib><creatorcontrib>Chen, Danni</creatorcontrib><creatorcontrib>Gu, Xidong</creatorcontrib><creatorcontrib>Li, Chenggong</creatorcontrib><creatorcontrib>Yao, Minya</creatorcontrib><creatorcontrib>Pan, Jie</creatorcontrib><creatorcontrib>Cheng, Junchi</creatorcontrib><creatorcontrib>Jiang, Donghai</creatorcontrib><creatorcontrib>Xu, Liang</creatorcontrib><creatorcontrib>Bao, Chang</creatorcontrib><creatorcontrib>Fu, Peifen</creatorcontrib><creatorcontrib>Fan, Weimin</creatorcontrib><collection>Springer Nature OA Free Journals</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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Si, Wengong</au><au>Shen, Jiaying</au><au>Du, Chengyong</au><au>Chen, Danni</au><au>Gu, Xidong</au><au>Li, Chenggong</au><au>Yao, Minya</au><au>Pan, Jie</au><au>Cheng, Junchi</au><au>Jiang, Donghai</au><au>Xu, Liang</au><au>Bao, Chang</au><au>Fu, Peifen</au><au>Fan, Weimin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A miR-20a/MAPK1/c-Myc regulatory feedback loop regulates breast carcinogenesis and chemoresistance</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>25</volume><issue>2</issue><spage>406</spage><epage>420</epage><pages>406-420</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Chemoresistance often leads to the failure of breast cancer treatment. MicroRNAs (miRNAs) play an important role in the progression and chemoresistance of cancer. However, because of the complexity of the mechanisms of chemoresistance and the specificity of miRNA regulation in different cell types, the function of miR-20a in breast cancer chemoresistance is still unclear. Here, by using miRNA microarray and high-content screening techniques, we found that miR-20a/b were significantly downregulated in breast cancer tissues compared with normal breast tissues, and low miR-20a/b expression was correlated with poor survival in breast cancer patients. Ectopic overexpression of miR-20a sensitized breast cancer cells to a broad spectrum of chemotherapy drugs and suppress their proliferation both
in vitro
and
in vivo
. Further study demonstrated that miR-20a directly targeted the 3'untranslated region of
MAPK1
, and thus downregulated the expression of P-gp and c-Myc by inhibiting the MAPK/ERK signaling pathway, whereas c-Myc can bind to the promoter region of the miR-20a gene to promote the expression of miR-20a. Together, our study identified a novel miR-20a/MAPK1/c-Myc feedback loop that regulates breast cancer growth and chemoresistance. These findings suggest that miR-20a synergizing with anticancer drugs will be a promising treatment strategy, especially for chemoresistant patients.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29125598</pmid><doi>10.1038/cdd.2017.176</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell death and differentiation, 2018-02, Vol.25 (2), p.406-420 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; SpringerLink Journals - AutoHoldings |
| subjects | 631/67/1857 692/420/2489/68 Antineoplastic Agents - pharmacology Antineoplastic drugs Antitumor agents Apoptosis Biochemistry Biomedical and Life Sciences Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Breast Neoplasms - pathology c-Myc protein Cancer therapies Carcinogenesis Cell Biology Cell Cycle Analysis Cell proliferation Cell Proliferation - drug effects Chemoresistance Chemotherapy DNA microarrays Drug Resistance, Neoplasm - drug effects Drug Screening Assays, Antitumor Feedback Feedback loops Female Humans Life Sciences MAP kinase MicroRNAs - genetics MicroRNAs - metabolism miRNA Mitogen-Activated Protein Kinase 1 - metabolism Myc protein Oligonucleotide Array Sequence Analysis Original Paper Proto-Oncogene Proteins c-myc - metabolism Signal transduction Stem Cells Tumor Cells, Cultured |
| title | A miR-20a/MAPK1/c-Myc regulatory feedback loop regulates breast carcinogenesis and chemoresistance |
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