SMAD2 Inactivation Inhibits CLDN6 Methylation to Suppress Migration and Invasion of Breast Cancer Cells
The downregulation of tight junction protein CLDN6 promotes breast cancer cell migration and invasion; however, the exact mechanism underlying CLDN6 downregulation remains unclear. CLDN6 silence is associated with DNA methyltransferase 1 (DNMT1) mediated DNA methylation, and DNMT1 is regulated by th...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2017-08, Vol.18 (9), p.1863 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 9 |
| container_start_page | 1863 |
| container_title | International journal of molecular sciences |
| container_volume | 18 |
| creator | Lu, Yan Wang, Liping Li, Hairi Li, Yanru Ruan, Yang Lin, Dongjing Yang, Minlan Jin, Xiangshu Guo, Yantong Zhang, Xiaoli Quan, Chengshi |
| description | The downregulation of tight junction protein CLDN6 promotes breast cancer cell migration and invasion; however, the exact mechanism underlying CLDN6 downregulation remains unclear. CLDN6 silence is associated with DNA methyltransferase 1 (DNMT1) mediated DNA methylation, and DNMT1 is regulated by the transforming growth factor beta (TGFβ)/SMAD pathway. Therefore, we hypothesized that TGFβ/SMAD pathway, specifically SMAD2, may play a critical role for CLDN6 downregulation through DNA methyltransferase 1 (DNMT1) mediated DNA methylation. To test this hypothesis, we blocked the SMAD2 pathway with SB431542 in two human breast cancer cell lines (MCF-7 and SKBR-3). Our results showed that treatment with SB431542 led to a decrease of DNMT1 expression and the binding activity for CLDN6 promoter. The methylation level of CLDN6 promoter was decreased, and simultaneously CLDN6 protein expression increased. Upregulation of CLDN6 inhibited epithelial to mesenchymal transition (EMT) and reduced the migration and invasion ability of both MCF-7 and SKBR-3 cells. Furthermore, knocked down of CLDN6 abolished SB431542 effects on suppression of EMT associated gene expression and inhibition of migration and invasion. Thus, we demonstrated that the downregulation of CLDN6 is regulated through promoter methylation by DNMT1, which depends on the SMAD2 pathway, and that CLDN6 is a key regulator in the SMAD2/DNMT1/CLDN6 pathway to inhibit EMT, migration and invasion of breast cancer cells. |
| doi_str_mv | 10.3390/ijms18091863 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5618512</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1952219517</sourcerecordid><originalsourceid>FETCH-LOGICAL-c478t-b07f1989d7feec9a56f6de32c93d2c59bafb9632e1fb580cacf307083218fab23</originalsourceid><addsrcrecordid>eNpdkc1LAzEQxYMotlZvnmXBiwer-WiyyUXQ9RNaPajnkM0mbcp2U5Nswf_eLVWpniaT-c1jHg-AYwQvCBHw0s0XEXEoEGdkB_TRCOMhhCzf3Xr3wEGMcwgxwVTsgx7mnOU5Q30wfZ1c3-LsqVE6uZVKzjddM3OlSzErxrfPLJuYNPusN6Pks9d2uQwmxmzipmHzq5qqW1qpuG68zW6CUTFlhWq0CVlh6joegj2r6miOvusAvN_fvRWPw_HLw1NxPR7qUc7TsIS5RYKLKrfGaKEos6wyBGtBKqypKJUtBSPYIFtSDrXSlsAccoIRt6rEZACuNrrLtlyYSpsmBVXLZXALFT6lV07-nTRuJqd-JSlDnKK1wNm3QPAfrYlJLlzUnQXVGN9GiQShRCBBUYee_kPnvg1NZ6-jKMZrKO-o8w2lg48xGPt7DIJynaDcTrDDT7YN_MI_kZEvYGiX9w</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1952219517</pqid></control><display><type>article</type><title>SMAD2 Inactivation Inhibits CLDN6 Methylation to Suppress Migration and Invasion of Breast Cancer Cells</title><source>Electronic Journals Library</source><source>PubMed Central (Open Access)</source><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><creator>Lu, Yan ; Wang, Liping ; Li, Hairi ; Li, Yanru ; Ruan, Yang ; Lin, Dongjing ; Yang, Minlan ; Jin, Xiangshu ; Guo, Yantong ; Zhang, Xiaoli ; Quan, Chengshi</creator><creatorcontrib>Lu, Yan ; Wang, Liping ; Li, Hairi ; Li, Yanru ; Ruan, Yang ; Lin, Dongjing ; Yang, Minlan ; Jin, Xiangshu ; Guo, Yantong ; Zhang, Xiaoli ; Quan, Chengshi</creatorcontrib><description>The downregulation of tight junction protein CLDN6 promotes breast cancer cell migration and invasion; however, the exact mechanism underlying CLDN6 downregulation remains unclear. CLDN6 silence is associated with DNA methyltransferase 1 (DNMT1) mediated DNA methylation, and DNMT1 is regulated by the transforming growth factor beta (TGFβ)/SMAD pathway. Therefore, we hypothesized that TGFβ/SMAD pathway, specifically SMAD2, may play a critical role for CLDN6 downregulation through DNA methyltransferase 1 (DNMT1) mediated DNA methylation. To test this hypothesis, we blocked the SMAD2 pathway with SB431542 in two human breast cancer cell lines (MCF-7 and SKBR-3). Our results showed that treatment with SB431542 led to a decrease of DNMT1 expression and the binding activity for CLDN6 promoter. The methylation level of CLDN6 promoter was decreased, and simultaneously CLDN6 protein expression increased. Upregulation of CLDN6 inhibited epithelial to mesenchymal transition (EMT) and reduced the migration and invasion ability of both MCF-7 and SKBR-3 cells. Furthermore, knocked down of CLDN6 abolished SB431542 effects on suppression of EMT associated gene expression and inhibition of migration and invasion. Thus, we demonstrated that the downregulation of CLDN6 is regulated through promoter methylation by DNMT1, which depends on the SMAD2 pathway, and that CLDN6 is a key regulator in the SMAD2/DNMT1/CLDN6 pathway to inhibit EMT, migration and invasion of breast cancer cells.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms18091863</identifier><identifier>PMID: 28867761</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cell Movement - genetics ; Cell Proliferation - genetics ; Claudins - antagonists & inhibitors ; Claudins - genetics ; Deoxyribonucleic acid ; DNA ; DNA (Cytosine-5-)-Methyltransferase 1 - genetics ; DNA methylation ; DNA Methylation - genetics ; DNA methyltransferase ; DNMT1 protein ; Epithelial-Mesenchymal Transition - genetics ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic - genetics ; Gene Knockdown Techniques ; Humans ; MCF-7 Cells ; Mesenchyme ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Signal Transduction - genetics ; Silence ; Smad protein ; Smad2 protein ; Smad2 Protein - genetics ; Transforming growth factor-b ; Tumor cell lines</subject><ispartof>International journal of molecular sciences, 2017-08, Vol.18 (9), p.1863</ispartof><rights>Copyright MDPI AG 2017</rights><rights>2017 by the authors. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-b07f1989d7feec9a56f6de32c93d2c59bafb9632e1fb580cacf307083218fab23</citedby><cites>FETCH-LOGICAL-c478t-b07f1989d7feec9a56f6de32c93d2c59bafb9632e1fb580cacf307083218fab23</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/PMC5618512/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5618512/$$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/28867761$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Yan</creatorcontrib><creatorcontrib>Wang, Liping</creatorcontrib><creatorcontrib>Li, Hairi</creatorcontrib><creatorcontrib>Li, Yanru</creatorcontrib><creatorcontrib>Ruan, Yang</creatorcontrib><creatorcontrib>Lin, Dongjing</creatorcontrib><creatorcontrib>Yang, Minlan</creatorcontrib><creatorcontrib>Jin, Xiangshu</creatorcontrib><creatorcontrib>Guo, Yantong</creatorcontrib><creatorcontrib>Zhang, Xiaoli</creatorcontrib><creatorcontrib>Quan, Chengshi</creatorcontrib><title>SMAD2 Inactivation Inhibits CLDN6 Methylation to Suppress Migration and Invasion of Breast Cancer Cells</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>The downregulation of tight junction protein CLDN6 promotes breast cancer cell migration and invasion; however, the exact mechanism underlying CLDN6 downregulation remains unclear. CLDN6 silence is associated with DNA methyltransferase 1 (DNMT1) mediated DNA methylation, and DNMT1 is regulated by the transforming growth factor beta (TGFβ)/SMAD pathway. Therefore, we hypothesized that TGFβ/SMAD pathway, specifically SMAD2, may play a critical role for CLDN6 downregulation through DNA methyltransferase 1 (DNMT1) mediated DNA methylation. To test this hypothesis, we blocked the SMAD2 pathway with SB431542 in two human breast cancer cell lines (MCF-7 and SKBR-3). Our results showed that treatment with SB431542 led to a decrease of DNMT1 expression and the binding activity for CLDN6 promoter. The methylation level of CLDN6 promoter was decreased, and simultaneously CLDN6 protein expression increased. Upregulation of CLDN6 inhibited epithelial to mesenchymal transition (EMT) and reduced the migration and invasion ability of both MCF-7 and SKBR-3 cells. Furthermore, knocked down of CLDN6 abolished SB431542 effects on suppression of EMT associated gene expression and inhibition of migration and invasion. Thus, we demonstrated that the downregulation of CLDN6 is regulated through promoter methylation by DNMT1, which depends on the SMAD2 pathway, and that CLDN6 is a key regulator in the SMAD2/DNMT1/CLDN6 pathway to inhibit EMT, migration and invasion of breast cancer cells.</description><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Claudins - antagonists & inhibitors</subject><subject>Claudins - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA (Cytosine-5-)-Methyltransferase 1 - genetics</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>DNA methyltransferase</subject><subject>DNMT1 protein</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>MCF-7 Cells</subject><subject>Mesenchyme</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Signal Transduction - genetics</subject><subject>Silence</subject><subject>Smad protein</subject><subject>Smad2 protein</subject><subject>Smad2 Protein - genetics</subject><subject>Transforming growth factor-b</subject><subject>Tumor cell lines</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1LAzEQxYMotlZvnmXBiwer-WiyyUXQ9RNaPajnkM0mbcp2U5Nswf_eLVWpniaT-c1jHg-AYwQvCBHw0s0XEXEoEGdkB_TRCOMhhCzf3Xr3wEGMcwgxwVTsgx7mnOU5Q30wfZ1c3-LsqVE6uZVKzjddM3OlSzErxrfPLJuYNPusN6Pks9d2uQwmxmzipmHzq5qqW1qpuG68zW6CUTFlhWq0CVlh6joegj2r6miOvusAvN_fvRWPw_HLw1NxPR7qUc7TsIS5RYKLKrfGaKEos6wyBGtBKqypKJUtBSPYIFtSDrXSlsAccoIRt6rEZACuNrrLtlyYSpsmBVXLZXALFT6lV07-nTRuJqd-JSlDnKK1wNm3QPAfrYlJLlzUnQXVGN9GiQShRCBBUYee_kPnvg1NZ6-jKMZrKO-o8w2lg48xGPt7DIJynaDcTrDDT7YN_MI_kZEvYGiX9w</recordid><startdate>20170830</startdate><enddate>20170830</enddate><creator>Lu, Yan</creator><creator>Wang, Liping</creator><creator>Li, Hairi</creator><creator>Li, Yanru</creator><creator>Ruan, Yang</creator><creator>Lin, Dongjing</creator><creator>Yang, Minlan</creator><creator>Jin, Xiangshu</creator><creator>Guo, Yantong</creator><creator>Zhang, Xiaoli</creator><creator>Quan, Chengshi</creator><general>MDPI AG</general><general>MDPI</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>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170830</creationdate><title>SMAD2 Inactivation Inhibits CLDN6 Methylation to Suppress Migration and Invasion of Breast Cancer Cells</title><author>Lu, Yan ; Wang, Liping ; Li, Hairi ; Li, Yanru ; Ruan, Yang ; Lin, Dongjing ; Yang, Minlan ; Jin, Xiangshu ; Guo, Yantong ; Zhang, Xiaoli ; Quan, Chengshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-b07f1989d7feec9a56f6de32c93d2c59bafb9632e1fb580cacf307083218fab23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Claudins - antagonists & inhibitors</topic><topic>Claudins - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA (Cytosine-5-)-Methyltransferase 1 - genetics</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>DNA methyltransferase</topic><topic>DNMT1 protein</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>MCF-7 Cells</topic><topic>Mesenchyme</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Signal Transduction - genetics</topic><topic>Silence</topic><topic>Smad protein</topic><topic>Smad2 protein</topic><topic>Smad2 Protein - genetics</topic><topic>Transforming growth factor-b</topic><topic>Tumor cell lines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Yan</creatorcontrib><creatorcontrib>Wang, Liping</creatorcontrib><creatorcontrib>Li, Hairi</creatorcontrib><creatorcontrib>Li, Yanru</creatorcontrib><creatorcontrib>Ruan, Yang</creatorcontrib><creatorcontrib>Lin, Dongjing</creatorcontrib><creatorcontrib>Yang, Minlan</creatorcontrib><creatorcontrib>Jin, Xiangshu</creatorcontrib><creatorcontrib>Guo, Yantong</creatorcontrib><creatorcontrib>Zhang, Xiaoli</creatorcontrib><creatorcontrib>Quan, Chengshi</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>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Yan</au><au>Wang, Liping</au><au>Li, Hairi</au><au>Li, Yanru</au><au>Ruan, Yang</au><au>Lin, Dongjing</au><au>Yang, Minlan</au><au>Jin, Xiangshu</au><au>Guo, Yantong</au><au>Zhang, Xiaoli</au><au>Quan, Chengshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SMAD2 Inactivation Inhibits CLDN6 Methylation to Suppress Migration and Invasion of Breast Cancer Cells</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2017-08-30</date><risdate>2017</risdate><volume>18</volume><issue>9</issue><spage>1863</spage><pages>1863-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The downregulation of tight junction protein CLDN6 promotes breast cancer cell migration and invasion; however, the exact mechanism underlying CLDN6 downregulation remains unclear. CLDN6 silence is associated with DNA methyltransferase 1 (DNMT1) mediated DNA methylation, and DNMT1 is regulated by the transforming growth factor beta (TGFβ)/SMAD pathway. Therefore, we hypothesized that TGFβ/SMAD pathway, specifically SMAD2, may play a critical role for CLDN6 downregulation through DNA methyltransferase 1 (DNMT1) mediated DNA methylation. To test this hypothesis, we blocked the SMAD2 pathway with SB431542 in two human breast cancer cell lines (MCF-7 and SKBR-3). Our results showed that treatment with SB431542 led to a decrease of DNMT1 expression and the binding activity for CLDN6 promoter. The methylation level of CLDN6 promoter was decreased, and simultaneously CLDN6 protein expression increased. Upregulation of CLDN6 inhibited epithelial to mesenchymal transition (EMT) and reduced the migration and invasion ability of both MCF-7 and SKBR-3 cells. Furthermore, knocked down of CLDN6 abolished SB431542 effects on suppression of EMT associated gene expression and inhibition of migration and invasion. Thus, we demonstrated that the downregulation of CLDN6 is regulated through promoter methylation by DNMT1, which depends on the SMAD2 pathway, and that CLDN6 is a key regulator in the SMAD2/DNMT1/CLDN6 pathway to inhibit EMT, migration and invasion of breast cancer cells.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>28867761</pmid><doi>10.3390/ijms18091863</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2017-08, Vol.18 (9), p.1863 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5618512 |
| source | Electronic Journals Library; PubMed Central (Open Access); MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE |
| subjects | Breast cancer Breast Neoplasms - genetics Breast Neoplasms - pathology Cell Movement - genetics Cell Proliferation - genetics Claudins - antagonists & inhibitors Claudins - genetics Deoxyribonucleic acid DNA DNA (Cytosine-5-)-Methyltransferase 1 - genetics DNA methylation DNA Methylation - genetics DNA methyltransferase DNMT1 protein Epithelial-Mesenchymal Transition - genetics Female Gene expression Gene Expression Regulation, Neoplastic - genetics Gene Knockdown Techniques Humans MCF-7 Cells Mesenchyme Neoplasm Invasiveness - genetics Neoplasm Invasiveness - pathology Signal Transduction - genetics Silence Smad protein Smad2 protein Smad2 Protein - genetics Transforming growth factor-b Tumor cell lines |
| title | SMAD2 Inactivation Inhibits CLDN6 Methylation to Suppress Migration and Invasion of 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=2025-02-14T13%3A27%3A17IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=SMAD2%20Inactivation%20Inhibits%20CLDN6%20Methylation%20to%20Suppress%20Migration%20and%20Invasion%20of%20Breast%20Cancer%20Cells&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Lu,%20Yan&rft.date=2017-08-30&rft.volume=18&rft.issue=9&rft.spage=1863&rft.pages=1863-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms18091863&rft_dat=%3Cproquest_pubme%3E1952219517%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1952219517&rft_id=info:pmid/28867761&rfr_iscdi=true |