Proteomic analysis of acquired tamoxifen resistance in MCF-7 cells reveals expression signatures associated with enhanced migration
Acquired tamoxifen resistance involves complex signaling events that are not yet fully understood. Successful therapeutic intervention to delay the onset of hormone resistance depends critically on mechanistic elucidation of viable molecular targets associated with hormone resistance. This study was...
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| Veröffentlicht in: | Breast cancer research : BCR 2012-03, Vol.14 (2), p.R45-R45, Article R45 |
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| creator | Zhou, Changhua Zhong, Qiu Rhodes, Lyndsay V Townley, Ian Bratton, Melyssa R Zhang, Qiang Martin, Elizabeth C Elliott, Steven Collins-Burow, Bridgette M Burow, Matthew E Wang, Guangdi |
| description | Acquired tamoxifen resistance involves complex signaling events that are not yet fully understood. Successful therapeutic intervention to delay the onset of hormone resistance depends critically on mechanistic elucidation of viable molecular targets associated with hormone resistance. This study was undertaken to investigate the global proteomic alterations in a tamoxifen resistant MCF-7 breast cancer cell line obtained by long term treatment of the wild type MCF-7 cell line with 4-hydroxytamoxifen (4-OH Tam).
We cultured MCF-7 cells with 4-OH Tam over a period of 12 months to obtain the resistant cell line. A gel-free, quantitative proteomic method was used to identify and quantify the proteome of the resistant cell line. Nano-flow high-performance liquid chromatography coupled to high resolution Fourier transform mass spectrometry was used to analyze fractionated peptide mixtures that were isobarically labeled from the resistant and control cell lysates. Real time quantitative PCR and Western blots were used to verify selected proteomic changes. Lentiviral vector transduction was used to generate MCF-7 cells stably expressing S100P. Online pathway analysis was performed to assess proteomic signatures in tamoxifen resistance. Survival analysis was done to evaluate clinical relevance of altered proteomic expressions.
Quantitative proteomic analysis revealed a wide breadth of signaling events during transition to acquired tamoxifen resistance. A total of 629 proteins were found significantly changed with 364 up-regulated and 265 down-regulated. Collectively, these changes demonstrated the suppressed state of estrogen receptor (ER) and ER-regulated genes, activated survival signaling and increased migratory capacity of the resistant cell line. The protein S100P was found to play a critical role in conferring tamoxifen resistance and enhanced cell motility.
Our data demonstrate that the adaptive changes in the proteome of tamoxifen resistant breast cancer cells are characterized by down-regulated ER signaling, activation of alternative survival pathways, and enhanced cell motility through regulation of the actin cytoskeleton dynamics. Evidence also emerged that S100P mediates acquired tamoxifen resistance and migration capacity. |
| doi_str_mv | 10.1186/bcr3144 |
| format | Article |
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We cultured MCF-7 cells with 4-OH Tam over a period of 12 months to obtain the resistant cell line. A gel-free, quantitative proteomic method was used to identify and quantify the proteome of the resistant cell line. Nano-flow high-performance liquid chromatography coupled to high resolution Fourier transform mass spectrometry was used to analyze fractionated peptide mixtures that were isobarically labeled from the resistant and control cell lysates. Real time quantitative PCR and Western blots were used to verify selected proteomic changes. Lentiviral vector transduction was used to generate MCF-7 cells stably expressing S100P. Online pathway analysis was performed to assess proteomic signatures in tamoxifen resistance. Survival analysis was done to evaluate clinical relevance of altered proteomic expressions.
Quantitative proteomic analysis revealed a wide breadth of signaling events during transition to acquired tamoxifen resistance. A total of 629 proteins were found significantly changed with 364 up-regulated and 265 down-regulated. Collectively, these changes demonstrated the suppressed state of estrogen receptor (ER) and ER-regulated genes, activated survival signaling and increased migratory capacity of the resistant cell line. The protein S100P was found to play a critical role in conferring tamoxifen resistance and enhanced cell motility.
Our data demonstrate that the adaptive changes in the proteome of tamoxifen resistant breast cancer cells are characterized by down-regulated ER signaling, activation of alternative survival pathways, and enhanced cell motility through regulation of the actin cytoskeleton dynamics. Evidence also emerged that S100P mediates acquired tamoxifen resistance and migration capacity.</description><identifier>ISSN: 1465-542X</identifier><identifier>ISSN: 1465-5411</identifier><identifier>EISSN: 1465-542X</identifier><identifier>DOI: 10.1186/bcr3144</identifier><identifier>PMID: 22417809</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Actin Cytoskeleton - metabolism ; Antineoplastic Agents, Hormonal - pharmacology ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - mortality ; Breast Neoplasms - pathology ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - metabolism ; Cancer cells ; Cell Line, Tumor ; Cell Movement ; Development and progression ; Down-Regulation - drug effects ; Drug Resistance, Neoplasm ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic aspects ; Health aspects ; Humans ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Physiological aspects ; Proteomics - methods ; Receptors, Estrogen - metabolism ; Signal Transduction - drug effects ; Tamoxifen ; Tamoxifen - pharmacology ; Tandem Mass Spectrometry</subject><ispartof>Breast cancer research : BCR, 2012-03, Vol.14 (2), p.R45-R45, Article R45</ispartof><rights>COPYRIGHT 2012 BioMed Central Ltd.</rights><rights>Copyright ©2012 Zhou et al.; licensee BioMed Central Ltd. 2012 Zhou et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b487t-a2930fda05f838e46b5d5ecf50a1d66773a922e14484062bb1df44e71246489e3</citedby><cites>FETCH-LOGICAL-b487t-a2930fda05f838e46b5d5ecf50a1d66773a922e14484062bb1df44e71246489e3</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/PMC3446379/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446379/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22417809$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Changhua</creatorcontrib><creatorcontrib>Zhong, Qiu</creatorcontrib><creatorcontrib>Rhodes, Lyndsay V</creatorcontrib><creatorcontrib>Townley, Ian</creatorcontrib><creatorcontrib>Bratton, Melyssa R</creatorcontrib><creatorcontrib>Zhang, Qiang</creatorcontrib><creatorcontrib>Martin, Elizabeth C</creatorcontrib><creatorcontrib>Elliott, Steven</creatorcontrib><creatorcontrib>Collins-Burow, Bridgette M</creatorcontrib><creatorcontrib>Burow, Matthew E</creatorcontrib><creatorcontrib>Wang, Guangdi</creatorcontrib><title>Proteomic analysis of acquired tamoxifen resistance in MCF-7 cells reveals expression signatures associated with enhanced migration</title><title>Breast cancer research : BCR</title><addtitle>Breast Cancer Res</addtitle><description>Acquired tamoxifen resistance involves complex signaling events that are not yet fully understood. Successful therapeutic intervention to delay the onset of hormone resistance depends critically on mechanistic elucidation of viable molecular targets associated with hormone resistance. This study was undertaken to investigate the global proteomic alterations in a tamoxifen resistant MCF-7 breast cancer cell line obtained by long term treatment of the wild type MCF-7 cell line with 4-hydroxytamoxifen (4-OH Tam).
We cultured MCF-7 cells with 4-OH Tam over a period of 12 months to obtain the resistant cell line. A gel-free, quantitative proteomic method was used to identify and quantify the proteome of the resistant cell line. Nano-flow high-performance liquid chromatography coupled to high resolution Fourier transform mass spectrometry was used to analyze fractionated peptide mixtures that were isobarically labeled from the resistant and control cell lysates. Real time quantitative PCR and Western blots were used to verify selected proteomic changes. Lentiviral vector transduction was used to generate MCF-7 cells stably expressing S100P. Online pathway analysis was performed to assess proteomic signatures in tamoxifen resistance. Survival analysis was done to evaluate clinical relevance of altered proteomic expressions.
Quantitative proteomic analysis revealed a wide breadth of signaling events during transition to acquired tamoxifen resistance. A total of 629 proteins were found significantly changed with 364 up-regulated and 265 down-regulated. Collectively, these changes demonstrated the suppressed state of estrogen receptor (ER) and ER-regulated genes, activated survival signaling and increased migratory capacity of the resistant cell line. The protein S100P was found to play a critical role in conferring tamoxifen resistance and enhanced cell motility.
Our data demonstrate that the adaptive changes in the proteome of tamoxifen resistant breast cancer cells are characterized by down-regulated ER signaling, activation of alternative survival pathways, and enhanced cell motility through regulation of the actin cytoskeleton dynamics. Evidence also emerged that S100P mediates acquired tamoxifen resistance and migration capacity.</description><subject>Actin Cytoskeleton - metabolism</subject><subject>Antineoplastic Agents, Hormonal - pharmacology</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - mortality</subject><subject>Breast Neoplasms - pathology</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Cancer cells</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Development and progression</subject><subject>Down-Regulation - drug effects</subject><subject>Drug Resistance, Neoplasm</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Physiological aspects</subject><subject>Proteomics - methods</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Tamoxifen</subject><subject>Tamoxifen - pharmacology</subject><subject>Tandem Mass Spectrometry</subject><issn>1465-542X</issn><issn>1465-5411</issn><issn>1465-542X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1Ut1rFDEQD6LYWsX_QAI--LRtvnY364NQDquFFn1Q8C3MZid3kd3kTPZq--w_bo6r5Q4seZhJfh_MZIaQ15ydcq6bs94myZV6Qo65auqqVuLH0738iLzI-SdjvNW1fk6OhFAlZd0x-fM1xRnj5C2FAONd9plGR8H-2viEA51hirfeYaAJCzZDsEh9oNeLi6qlFscxF-QGoUS8XRdS9jHQ7JcB5k25Usg5Wg9zMfvt5xXFsNqaDHTyywRzYb8kz1zR46v7eEK-X3z8tvhcXX35dLk4v6p6pdu5AtFJ5gZgtdNSo2r6eqjRupoBH5qmbSV0QmD5Bq1YI_qeD04pbLlQjdIdyhPyYee73vQTDhbDnGA06-QnSHcmgjeHSPArs4w3RirVyLYrBu93Br2PjxgcIjZO5n40Rfx2J17CiMYHFwvFTj5bcy50LbcdbFmn_2GVM2CZUQzofHk_ELzbCWyKOSd0D-VwZra7sVfAm_32H3j_lkH-BVF_uQ4</recordid><startdate>20120314</startdate><enddate>20120314</enddate><creator>Zhou, Changhua</creator><creator>Zhong, Qiu</creator><creator>Rhodes, Lyndsay V</creator><creator>Townley, Ian</creator><creator>Bratton, Melyssa R</creator><creator>Zhang, Qiang</creator><creator>Martin, Elizabeth C</creator><creator>Elliott, Steven</creator><creator>Collins-Burow, Bridgette M</creator><creator>Burow, Matthew E</creator><creator>Wang, Guangdi</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>5PM</scope></search><sort><creationdate>20120314</creationdate><title>Proteomic analysis of acquired tamoxifen resistance in MCF-7 cells reveals expression signatures associated with enhanced migration</title><author>Zhou, Changhua ; Zhong, Qiu ; Rhodes, Lyndsay V ; Townley, Ian ; Bratton, Melyssa R ; Zhang, Qiang ; Martin, Elizabeth C ; Elliott, Steven ; Collins-Burow, Bridgette M ; Burow, Matthew E ; Wang, Guangdi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b487t-a2930fda05f838e46b5d5ecf50a1d66773a922e14484062bb1df44e71246489e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Actin Cytoskeleton - metabolism</topic><topic>Antineoplastic Agents, Hormonal - pharmacology</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - mortality</topic><topic>Breast Neoplasms - pathology</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Cancer cells</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Development and progression</topic><topic>Down-Regulation - drug effects</topic><topic>Drug Resistance, Neoplasm</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Physiological aspects</topic><topic>Proteomics - methods</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Tamoxifen</topic><topic>Tamoxifen - pharmacology</topic><topic>Tandem Mass Spectrometry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Changhua</creatorcontrib><creatorcontrib>Zhong, Qiu</creatorcontrib><creatorcontrib>Rhodes, Lyndsay V</creatorcontrib><creatorcontrib>Townley, Ian</creatorcontrib><creatorcontrib>Bratton, Melyssa R</creatorcontrib><creatorcontrib>Zhang, Qiang</creatorcontrib><creatorcontrib>Martin, Elizabeth C</creatorcontrib><creatorcontrib>Elliott, Steven</creatorcontrib><creatorcontrib>Collins-Burow, Bridgette M</creatorcontrib><creatorcontrib>Burow, Matthew E</creatorcontrib><creatorcontrib>Wang, Guangdi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Breast cancer research : BCR</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Changhua</au><au>Zhong, Qiu</au><au>Rhodes, Lyndsay V</au><au>Townley, Ian</au><au>Bratton, Melyssa R</au><au>Zhang, Qiang</au><au>Martin, Elizabeth C</au><au>Elliott, Steven</au><au>Collins-Burow, Bridgette M</au><au>Burow, Matthew E</au><au>Wang, Guangdi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proteomic analysis of acquired tamoxifen resistance in MCF-7 cells reveals expression signatures associated with enhanced migration</atitle><jtitle>Breast cancer research : BCR</jtitle><addtitle>Breast Cancer Res</addtitle><date>2012-03-14</date><risdate>2012</risdate><volume>14</volume><issue>2</issue><spage>R45</spage><epage>R45</epage><pages>R45-R45</pages><artnum>R45</artnum><issn>1465-542X</issn><issn>1465-5411</issn><eissn>1465-542X</eissn><abstract>Acquired tamoxifen resistance involves complex signaling events that are not yet fully understood. Successful therapeutic intervention to delay the onset of hormone resistance depends critically on mechanistic elucidation of viable molecular targets associated with hormone resistance. This study was undertaken to investigate the global proteomic alterations in a tamoxifen resistant MCF-7 breast cancer cell line obtained by long term treatment of the wild type MCF-7 cell line with 4-hydroxytamoxifen (4-OH Tam).
We cultured MCF-7 cells with 4-OH Tam over a period of 12 months to obtain the resistant cell line. A gel-free, quantitative proteomic method was used to identify and quantify the proteome of the resistant cell line. Nano-flow high-performance liquid chromatography coupled to high resolution Fourier transform mass spectrometry was used to analyze fractionated peptide mixtures that were isobarically labeled from the resistant and control cell lysates. Real time quantitative PCR and Western blots were used to verify selected proteomic changes. Lentiviral vector transduction was used to generate MCF-7 cells stably expressing S100P. Online pathway analysis was performed to assess proteomic signatures in tamoxifen resistance. Survival analysis was done to evaluate clinical relevance of altered proteomic expressions.
Quantitative proteomic analysis revealed a wide breadth of signaling events during transition to acquired tamoxifen resistance. A total of 629 proteins were found significantly changed with 364 up-regulated and 265 down-regulated. Collectively, these changes demonstrated the suppressed state of estrogen receptor (ER) and ER-regulated genes, activated survival signaling and increased migratory capacity of the resistant cell line. The protein S100P was found to play a critical role in conferring tamoxifen resistance and enhanced cell motility.
Our data demonstrate that the adaptive changes in the proteome of tamoxifen resistant breast cancer cells are characterized by down-regulated ER signaling, activation of alternative survival pathways, and enhanced cell motility through regulation of the actin cytoskeleton dynamics. Evidence also emerged that S100P mediates acquired tamoxifen resistance and migration capacity.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>22417809</pmid><doi>10.1186/bcr3144</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; SpringerNature Complete Journals; PubMed Central Open Access; Springer Nature OA Free Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Actin Cytoskeleton - metabolism Antineoplastic Agents, Hormonal - pharmacology Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - mortality Breast Neoplasms - pathology Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Cancer cells Cell Line, Tumor Cell Movement Development and progression Down-Regulation - drug effects Drug Resistance, Neoplasm Female Gene expression Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Health aspects Humans Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Physiological aspects Proteomics - methods Receptors, Estrogen - metabolism Signal Transduction - drug effects Tamoxifen Tamoxifen - pharmacology Tandem Mass Spectrometry |
| title | Proteomic analysis of acquired tamoxifen resistance in MCF-7 cells reveals expression signatures associated with enhanced migration |
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