Bisphenol AF-induced endogenous transcription is mediated by ERα and ERK1/2 activation in human breast cancer cells
Bisphenol AF (BPAF)-induced transcriptional activity has been evaluated by luciferase reporter assay. However, the molecular mechanism of BPAF-induced endogenous transcription in human breast cancer cells has not been fully elucidated. In the present study, we investigated the effect and mechanism o...
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| description | Bisphenol AF (BPAF)-induced transcriptional activity has been evaluated by luciferase reporter assay. However, the molecular mechanism of BPAF-induced endogenous transcription in human breast cancer cells has not been fully elucidated. In the present study, we investigated the effect and mechanism of BPAF-induced endogenous transcription detected by real-time PCR in human breast cancer cells. We found that BPAF stimulated transcription of estrogen responsive genes, such as trefoil factor 1 (TFF1), growth regulation by estrogen in breast cancer 1 (GREB1) and cathepsin D (CTSD), through dose-dependent and time-dependent manners in T47D and MCF7 cells. Gene-silencing of ERα, ERβ and G protein-coupled estrogen receptor 1 (GPER) by small interfering RNA revealed that BPAF-induced endogenous transcription was dependent on ERα and GPER, implying both genomic and nongenomic pathways might be involved in the endogenous transcription induced by BPAF. ERα-mediated gene transcription was further confirmed by inhibition of ER activity using ICI 182780 in ERα-positive T47D and MCF7 cells as well as overexpression of ERα in ERα-negative MDA-MB-231 breast cancer cells. Moreover, we utilized Src tyrosine kinase inhibitor PP2 and two MEK inhibitors PD98059 and U0126 to elucidate the rapid nongenomic activation of Src/MEK/ERK1/2 cascade on endogenous transcription. Our data showed that BPAF-induced transcription could be significantly blocked by PP2, PD98059 and U0126, suggesting activation of ERK1/2 was also required to regulate endogenous transcription. Taken together, these results indicate that BPAF-induced endogenous transcription of estrogen responsive genes is mediated through both genomic and nongenomic pathways involving the ERα and ERK1/2 activation in human breast cancer cells. |
| doi_str_mv | 10.1371/journal.pone.0094725 |
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However, the molecular mechanism of BPAF-induced endogenous transcription in human breast cancer cells has not been fully elucidated. In the present study, we investigated the effect and mechanism of BPAF-induced endogenous transcription detected by real-time PCR in human breast cancer cells. We found that BPAF stimulated transcription of estrogen responsive genes, such as trefoil factor 1 (TFF1), growth regulation by estrogen in breast cancer 1 (GREB1) and cathepsin D (CTSD), through dose-dependent and time-dependent manners in T47D and MCF7 cells. Gene-silencing of ERα, ERβ and G protein-coupled estrogen receptor 1 (GPER) by small interfering RNA revealed that BPAF-induced endogenous transcription was dependent on ERα and GPER, implying both genomic and nongenomic pathways might be involved in the endogenous transcription induced by BPAF. ERα-mediated gene transcription was further confirmed by inhibition of ER activity using ICI 182780 in ERα-positive T47D and MCF7 cells as well as overexpression of ERα in ERα-negative MDA-MB-231 breast cancer cells. Moreover, we utilized Src tyrosine kinase inhibitor PP2 and two MEK inhibitors PD98059 and U0126 to elucidate the rapid nongenomic activation of Src/MEK/ERK1/2 cascade on endogenous transcription. Our data showed that BPAF-induced transcription could be significantly blocked by PP2, PD98059 and U0126, suggesting activation of ERK1/2 was also required to regulate endogenous transcription. Taken together, these results indicate that BPAF-induced endogenous transcription of estrogen responsive genes is mediated through both genomic and nongenomic pathways involving the ERα and ERK1/2 activation in human breast cancer cells.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0094725</identifier><identifier>PMID: 24727858</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Benzhydryl Compounds - pharmacology ; Binding sites ; Biology and Life Sciences ; Bisphenol A ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Cancer ; Cathepsin D ; Cell cycle ; Cell Line, Tumor ; Disease control ; Disease prevention ; Enzyme Activation ; Enzyme inhibitors ; Epidermal growth factor ; Estrogen Receptor alpha - metabolism ; Estrogen receptors ; Estrogens ; Extracellular signal-regulated kinase ; Female ; Food contamination & poisoning ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Genes ; Humans ; Insulin ; Kinases ; Laboratories ; Ligands ; MEK inhibitors ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Phenols ; Phenols - pharmacology ; Physical Sciences ; Protein-tyrosine kinase ; Proteins ; Proto-Oncogene Proteins B-raf - metabolism ; Public health ; Receptors, Estrogen - metabolism ; Receptors, G-Protein-Coupled - metabolism ; Ribonucleic acid ; RNA ; siRNA ; Src protein ; Transcription ; Transcription, Genetic ; Trefoil factor ; Tyrosine</subject><ispartof>PloS one, 2014-04, Vol.9 (4), p.e94725</ispartof><rights>2014 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Li et al 2014 Li et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-79a53da79fd258019b8555a29b55e376c099b0de084e17d29e0425303dd1ff623</citedby><cites>FETCH-LOGICAL-c526t-79a53da79fd258019b8555a29b55e376c099b0de084e17d29e0425303dd1ff623</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/PMC3984236/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3984236/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24727858$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Guo, Jing</creatorcontrib><creatorcontrib>Gao, Wenhui</creatorcontrib><creatorcontrib>Yu, Jianlong</creatorcontrib><creatorcontrib>Han, Xiaoyu</creatorcontrib><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Shao, Bing</creatorcontrib><title>Bisphenol AF-induced endogenous transcription is mediated by ERα and ERK1/2 activation in human breast cancer cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Bisphenol AF (BPAF)-induced transcriptional activity has been evaluated by luciferase reporter assay. However, the molecular mechanism of BPAF-induced endogenous transcription in human breast cancer cells has not been fully elucidated. In the present study, we investigated the effect and mechanism of BPAF-induced endogenous transcription detected by real-time PCR in human breast cancer cells. We found that BPAF stimulated transcription of estrogen responsive genes, such as trefoil factor 1 (TFF1), growth regulation by estrogen in breast cancer 1 (GREB1) and cathepsin D (CTSD), through dose-dependent and time-dependent manners in T47D and MCF7 cells. Gene-silencing of ERα, ERβ and G protein-coupled estrogen receptor 1 (GPER) by small interfering RNA revealed that BPAF-induced endogenous transcription was dependent on ERα and GPER, implying both genomic and nongenomic pathways might be involved in the endogenous transcription induced by BPAF. ERα-mediated gene transcription was further confirmed by inhibition of ER activity using ICI 182780 in ERα-positive T47D and MCF7 cells as well as overexpression of ERα in ERα-negative MDA-MB-231 breast cancer cells. Moreover, we utilized Src tyrosine kinase inhibitor PP2 and two MEK inhibitors PD98059 and U0126 to elucidate the rapid nongenomic activation of Src/MEK/ERK1/2 cascade on endogenous transcription. Our data showed that BPAF-induced transcription could be significantly blocked by PP2, PD98059 and U0126, suggesting activation of ERK1/2 was also required to regulate endogenous transcription. Taken together, these results indicate that BPAF-induced endogenous transcription of estrogen responsive genes is mediated through both genomic and nongenomic pathways involving the ERα and ERK1/2 activation in human breast cancer cells.</description><subject>Activation</subject><subject>Benzhydryl Compounds - pharmacology</subject><subject>Binding sites</subject><subject>Biology and Life Sciences</subject><subject>Bisphenol A</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer</subject><subject>Cathepsin D</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Disease control</subject><subject>Disease prevention</subject><subject>Enzyme Activation</subject><subject>Enzyme inhibitors</subject><subject>Epidermal growth factor</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Extracellular signal-regulated kinase</subject><subject>Female</subject><subject>Food contamination & poisoning</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes</subject><subject>Humans</subject><subject>Insulin</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Ligands</subject><subject>MEK inhibitors</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Phenols</subject><subject>Phenols - pharmacology</subject><subject>Physical Sciences</subject><subject>Protein-tyrosine kinase</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins B-raf - metabolism</subject><subject>Public health</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>siRNA</subject><subject>Src protein</subject><subject>Transcription</subject><subject>Transcription, Genetic</subject><subject>Trefoil factor</subject><subject>Tyrosine</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNp1Ut1qFDEUHkSxtfYNRANezzY_k8nkRqil1WKhUOx1OJNkdrPMJmOSKfSxfBGfydSdlvbCqxxOvp_Dx1dVHwheESbIyTbM0cO4moK3K4xlIyh_VR0SyWjdUsxeP5sPqncpbTHmrGvbt9UBLWDR8e6wyl9dmjbWhxGdXtTOm1lbg6w3YV2Wc0I5gk86uim74JFLaGeNg1xA_T06v_nzG4E3ZfhBTigCnd0d7JEebeYdeNRHCykjDV7biLQdx_S-ejPAmOzx8h5VtxfnP8--11fX3y7PTq9qzWmbayGBMwNCDobyDhPZd5xzoLLn3DLRaixlj43FXWOJMFRa3FDOMDOGDENL2VH1aa87jSGpJbCkCCecSiIEK4jLPcIE2Kopuh3EexXAqX-LENcKYnZ6tKo4E9EOnDZcN9Qy2XDQpNNa8qJkoGh9WdzmvoSkrS_ZjS9EX_54t1HrcKeY7BrK2iLweRGI4ddsU_7Pyc0epWNIKdrhyYFg9dCMR5Z6aIZamlFoH59f90R6rAL7C_0Lt5M</recordid><startdate>20140411</startdate><enddate>20140411</enddate><creator>Li, Ming</creator><creator>Guo, Jing</creator><creator>Gao, Wenhui</creator><creator>Yu, Jianlong</creator><creator>Han, Xiaoyu</creator><creator>Zhang, Jing</creator><creator>Shao, Bing</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140411</creationdate><title>Bisphenol AF-induced endogenous transcription is mediated by ERα and ERK1/2 activation in human breast cancer cells</title><author>Li, Ming ; Guo, Jing ; Gao, Wenhui ; Yu, Jianlong ; Han, Xiaoyu ; Zhang, Jing ; Shao, Bing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-79a53da79fd258019b8555a29b55e376c099b0de084e17d29e0425303dd1ff623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Activation</topic><topic>Benzhydryl Compounds - pharmacology</topic><topic>Binding sites</topic><topic>Biology and Life Sciences</topic><topic>Bisphenol A</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cancer</topic><topic>Cathepsin D</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Disease control</topic><topic>Disease prevention</topic><topic>Enzyme Activation</topic><topic>Enzyme inhibitors</topic><topic>Epidermal growth factor</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Extracellular signal-regulated kinase</topic><topic>Female</topic><topic>Food contamination & poisoning</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes</topic><topic>Humans</topic><topic>Insulin</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Ligands</topic><topic>MEK inhibitors</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Phenols</topic><topic>Phenols - pharmacology</topic><topic>Physical Sciences</topic><topic>Protein-tyrosine kinase</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins B-raf - metabolism</topic><topic>Public health</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>siRNA</topic><topic>Src protein</topic><topic>Transcription</topic><topic>Transcription, Genetic</topic><topic>Trefoil factor</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Guo, Jing</creatorcontrib><creatorcontrib>Gao, Wenhui</creatorcontrib><creatorcontrib>Yu, Jianlong</creatorcontrib><creatorcontrib>Han, Xiaoyu</creatorcontrib><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Shao, Bing</creatorcontrib><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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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However, the molecular mechanism of BPAF-induced endogenous transcription in human breast cancer cells has not been fully elucidated. In the present study, we investigated the effect and mechanism of BPAF-induced endogenous transcription detected by real-time PCR in human breast cancer cells. We found that BPAF stimulated transcription of estrogen responsive genes, such as trefoil factor 1 (TFF1), growth regulation by estrogen in breast cancer 1 (GREB1) and cathepsin D (CTSD), through dose-dependent and time-dependent manners in T47D and MCF7 cells. Gene-silencing of ERα, ERβ and G protein-coupled estrogen receptor 1 (GPER) by small interfering RNA revealed that BPAF-induced endogenous transcription was dependent on ERα and GPER, implying both genomic and nongenomic pathways might be involved in the endogenous transcription induced by BPAF. ERα-mediated gene transcription was further confirmed by inhibition of ER activity using ICI 182780 in ERα-positive T47D and MCF7 cells as well as overexpression of ERα in ERα-negative MDA-MB-231 breast cancer cells. Moreover, we utilized Src tyrosine kinase inhibitor PP2 and two MEK inhibitors PD98059 and U0126 to elucidate the rapid nongenomic activation of Src/MEK/ERK1/2 cascade on endogenous transcription. Our data showed that BPAF-induced transcription could be significantly blocked by PP2, PD98059 and U0126, suggesting activation of ERK1/2 was also required to regulate endogenous transcription. Taken together, these results indicate that BPAF-induced endogenous transcription of estrogen responsive genes is mediated through both genomic and nongenomic pathways involving the ERα and ERK1/2 activation in human breast cancer cells.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24727858</pmid><doi>10.1371/journal.pone.0094725</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Activation Benzhydryl Compounds - pharmacology Binding sites Biology and Life Sciences Bisphenol A Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer Cathepsin D Cell cycle Cell Line, Tumor Disease control Disease prevention Enzyme Activation Enzyme inhibitors Epidermal growth factor Estrogen Receptor alpha - metabolism Estrogen receptors Estrogens Extracellular signal-regulated kinase Female Food contamination & poisoning Gene expression Gene Expression Regulation, Neoplastic - drug effects Genes Humans Insulin Kinases Laboratories Ligands MEK inhibitors Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Phenols Phenols - pharmacology Physical Sciences Protein-tyrosine kinase Proteins Proto-Oncogene Proteins B-raf - metabolism Public health Receptors, Estrogen - metabolism Receptors, G-Protein-Coupled - metabolism Ribonucleic acid RNA siRNA Src protein Transcription Transcription, Genetic Trefoil factor Tyrosine |
| title | Bisphenol AF-induced endogenous transcription is mediated by ERα and ERK1/2 activation in human breast cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T22%3A58%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Bisphenol%20AF-induced%20endogenous%20transcription%20is%20mediated%20by%20ER%CE%B1%20and%20ERK1/2%20activation%20in%20human%20breast%20cancer%20cells&rft.jtitle=PloS%20one&rft.au=Li,%20Ming&rft.date=2014-04-11&rft.volume=9&rft.issue=4&rft.spage=e94725&rft.pages=e94725-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0094725&rft_dat=%3Cproquest_plos_%3E3273105861%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1515291773&rft_id=info:pmid/24727858&rft_doaj_id=oai_doaj_org_article_55a176f5245c42e3945ac18cc95773da&rfr_iscdi=true |