ABCB4 is frequently epigenetically silenced in human cancers and inhibits tumor growth
Epigenetic silencing through promoter hypermethylation is an important hallmark for the inactivation of tumor-related genes in carcinogenesis. Here we identified the ATP-binding cassette sub-family B member 4 (ABCB4) as a novel epigenetically silenced target gene. We investigated the epigenetic regu...
Gespeichert in:
| Veröffentlicht in: | Scientific reports 2014-11, Vol.4 (1), p.6899, Article 6899 |
|---|---|
| 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 | 1 |
| container_start_page | 6899 |
| container_title | Scientific reports |
| container_volume | 4 |
| creator | Kiehl, Steffen Herkt, Stefanie C. Richter, Antje M. Fuhrmann, Liesa El-Nikhely, Nefertiti Seeger, Werner Savai, Rajkumar Dammann, Reinhard H. |
| description | Epigenetic silencing through promoter hypermethylation is an important hallmark for the inactivation of tumor-related genes in carcinogenesis. Here we identified the
ATP-binding cassette sub-family B member 4 (ABCB4)
as a novel epigenetically silenced target gene. We investigated the epigenetic regulation of
ABCB4
in 26 human lung, breast, skin, liver, head and neck cancer cells lines and in primary cancers by methylation and expression analysis. Hypermethylation of the
ABCB4
CpG island promoter occurred in 16 out of 26 (62%) human cancer cell lines. Aberrant methylation of
ABCB4
was also revealed in 39% of primary lung cancer and in 20% of head and neck cancer tissues. In 37% of primary lung cancer samples, ABCB4 expression was absent. For breast cancer a significant hypermethylation occurred in tumor tissues (41%) compared to matching normal samples (0%, p = 0.002). Silencing of
ABCB4
was reversed by 5-aza-2'-deoxycytidine and zebularine treatments leading to its reexpression in cancer cells. Overexpression of ABCB4 significantly suppressed colony formation and proliferation of lung cancer cells. Hypermethylation of
Abcb4
occurred also in murine cancer, but was not found in normal tissues. Our findings suggest that
ABCB4
is a frequently silenced gene in different cancers and it may act tumor suppressivly in lung cancer. |
| doi_str_mv | 10.1038/srep06899 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4219162</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1898173098</sourcerecordid><originalsourceid>FETCH-LOGICAL-c504t-a582d0ebf40b03f7182052b57c76c659afe071e7a6bb1a596829d78a53643dc53</originalsourceid><addsrcrecordid>eNplkV1LwzAUhoMobsxd-Ack4JVCNUmbNrkR3PALBt6otyFN0zajTWfSKvv3ZmyOiblJTs7De95zDgDnGN1gFLNb7_QKpYzzIzAmKKERiQk5PniPwNT7JQqHEp5gfgpGhMZplsZoDD7uZ_NZAo2HpdOfg7Z9s4Z6ZSptdW-UbELoTaOt0gU0FtZDKy1UMsTOQ2k3n7XJTe9hP7Sdg5Xrvvv6DJyUsvF6ursn4P3x4W3-HC1en17m94tIUZT0kaSMFEjnZYJyFJcZZiSYzGmmslSllMtSowzrTKZ5jiXlKSO8yJgM9pO4UDSegLut7mrIW12o4N_JRqycaaVbi04a8TdjTS2q7kskBHOckiBwuRNwXWjf92LZDc4GzwIzznAWI84CdbWllOt8GHi5r4CR2GxB7LcQ2ItDS3vyd-YBuN4CPqRspd1ByX9qP_pZkco</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1898173098</pqid></control><display><type>article</type><title>ABCB4 is frequently epigenetically silenced in human cancers and inhibits tumor growth</title><source>MEDLINE</source><source>Nature Free</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>Springer Nature OA Free Journals</source><creator>Kiehl, Steffen ; Herkt, Stefanie C. ; Richter, Antje M. ; Fuhrmann, Liesa ; El-Nikhely, Nefertiti ; Seeger, Werner ; Savai, Rajkumar ; Dammann, Reinhard H.</creator><creatorcontrib>Kiehl, Steffen ; Herkt, Stefanie C. ; Richter, Antje M. ; Fuhrmann, Liesa ; El-Nikhely, Nefertiti ; Seeger, Werner ; Savai, Rajkumar ; Dammann, Reinhard H.</creatorcontrib><description>Epigenetic silencing through promoter hypermethylation is an important hallmark for the inactivation of tumor-related genes in carcinogenesis. Here we identified the
ATP-binding cassette sub-family B member 4 (ABCB4)
as a novel epigenetically silenced target gene. We investigated the epigenetic regulation of
ABCB4
in 26 human lung, breast, skin, liver, head and neck cancer cells lines and in primary cancers by methylation and expression analysis. Hypermethylation of the
ABCB4
CpG island promoter occurred in 16 out of 26 (62%) human cancer cell lines. Aberrant methylation of
ABCB4
was also revealed in 39% of primary lung cancer and in 20% of head and neck cancer tissues. In 37% of primary lung cancer samples, ABCB4 expression was absent. For breast cancer a significant hypermethylation occurred in tumor tissues (41%) compared to matching normal samples (0%, p = 0.002). Silencing of
ABCB4
was reversed by 5-aza-2'-deoxycytidine and zebularine treatments leading to its reexpression in cancer cells. Overexpression of ABCB4 significantly suppressed colony formation and proliferation of lung cancer cells. Hypermethylation of
Abcb4
occurred also in murine cancer, but was not found in normal tissues. Our findings suggest that
ABCB4
is a frequently silenced gene in different cancers and it may act tumor suppressivly in lung cancer.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep06899</identifier><identifier>PMID: 25367630</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/106 ; 13/109 ; 14/1 ; 14/105 ; 38/22 ; 38/39 ; 38/77 ; 38/90 ; 45/88 ; 5-aza-2'-deoxycytidine ; 631/208/176 ; 692/699/67/68 ; Animals ; ATP Binding Cassette Transporter, Sub-Family B - genetics ; ATP Binding Cassette Transporter, Sub-Family B - metabolism ; Breast cancer ; Carcinogenesis ; Cell Proliferation ; CpG Islands ; DNA Methylation ; Epigenesis, Genetic ; Epigenetics ; Gene Expression Regulation, Neoplastic ; Head & neck cancer ; HEK293 Cells ; HeLa Cells ; Humanities and Social Sciences ; Humans ; Inactivation ; Liver ; Liver cancer ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Methylation ; Mice ; Mice, Inbred C57BL ; multidisciplinary ; Science ; Skin ; Tumor cell lines ; Tumors</subject><ispartof>Scientific reports, 2014-11, Vol.4 (1), p.6899, Article 6899</ispartof><rights>The Author(s) 2014</rights><rights>Copyright Nature Publishing Group Nov 2014</rights><rights>Copyright © 2014, Macmillan Publishers Limited. All rights reserved 2014 Macmillan Publishers Limited. All rights reserved</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-a582d0ebf40b03f7182052b57c76c659afe071e7a6bb1a596829d78a53643dc53</citedby><cites>FETCH-LOGICAL-c504t-a582d0ebf40b03f7182052b57c76c659afe071e7a6bb1a596829d78a53643dc53</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/PMC4219162/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219162/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25367630$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kiehl, Steffen</creatorcontrib><creatorcontrib>Herkt, Stefanie C.</creatorcontrib><creatorcontrib>Richter, Antje M.</creatorcontrib><creatorcontrib>Fuhrmann, Liesa</creatorcontrib><creatorcontrib>El-Nikhely, Nefertiti</creatorcontrib><creatorcontrib>Seeger, Werner</creatorcontrib><creatorcontrib>Savai, Rajkumar</creatorcontrib><creatorcontrib>Dammann, Reinhard H.</creatorcontrib><title>ABCB4 is frequently epigenetically silenced in human cancers and inhibits tumor growth</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Epigenetic silencing through promoter hypermethylation is an important hallmark for the inactivation of tumor-related genes in carcinogenesis. Here we identified the
ATP-binding cassette sub-family B member 4 (ABCB4)
as a novel epigenetically silenced target gene. We investigated the epigenetic regulation of
ABCB4
in 26 human lung, breast, skin, liver, head and neck cancer cells lines and in primary cancers by methylation and expression analysis. Hypermethylation of the
ABCB4
CpG island promoter occurred in 16 out of 26 (62%) human cancer cell lines. Aberrant methylation of
ABCB4
was also revealed in 39% of primary lung cancer and in 20% of head and neck cancer tissues. In 37% of primary lung cancer samples, ABCB4 expression was absent. For breast cancer a significant hypermethylation occurred in tumor tissues (41%) compared to matching normal samples (0%, p = 0.002). Silencing of
ABCB4
was reversed by 5-aza-2'-deoxycytidine and zebularine treatments leading to its reexpression in cancer cells. Overexpression of ABCB4 significantly suppressed colony formation and proliferation of lung cancer cells. Hypermethylation of
Abcb4
occurred also in murine cancer, but was not found in normal tissues. Our findings suggest that
ABCB4
is a frequently silenced gene in different cancers and it may act tumor suppressivly in lung cancer.</description><subject>13/106</subject><subject>13/109</subject><subject>14/1</subject><subject>14/105</subject><subject>38/22</subject><subject>38/39</subject><subject>38/77</subject><subject>38/90</subject><subject>45/88</subject><subject>5-aza-2'-deoxycytidine</subject><subject>631/208/176</subject><subject>692/699/67/68</subject><subject>Animals</subject><subject>ATP Binding Cassette Transporter, Sub-Family B - genetics</subject><subject>ATP Binding Cassette Transporter, Sub-Family B - metabolism</subject><subject>Breast cancer</subject><subject>Carcinogenesis</subject><subject>Cell Proliferation</subject><subject>CpG Islands</subject><subject>DNA Methylation</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Head & neck cancer</subject><subject>HEK293 Cells</subject><subject>HeLa Cells</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Inactivation</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Methylation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>multidisciplinary</subject><subject>Science</subject><subject>Skin</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNplkV1LwzAUhoMobsxd-Ack4JVCNUmbNrkR3PALBt6otyFN0zajTWfSKvv3ZmyOiblJTs7De95zDgDnGN1gFLNb7_QKpYzzIzAmKKERiQk5PniPwNT7JQqHEp5gfgpGhMZplsZoDD7uZ_NZAo2HpdOfg7Z9s4Z6ZSptdW-UbELoTaOt0gU0FtZDKy1UMsTOQ2k3n7XJTe9hP7Sdg5Xrvvv6DJyUsvF6ursn4P3x4W3-HC1en17m94tIUZT0kaSMFEjnZYJyFJcZZiSYzGmmslSllMtSowzrTKZ5jiXlKSO8yJgM9pO4UDSegLut7mrIW12o4N_JRqycaaVbi04a8TdjTS2q7kskBHOckiBwuRNwXWjf92LZDc4GzwIzznAWI84CdbWllOt8GHi5r4CR2GxB7LcQ2ItDS3vyd-YBuN4CPqRspd1ByX9qP_pZkco</recordid><startdate>20141104</startdate><enddate>20141104</enddate><creator>Kiehl, Steffen</creator><creator>Herkt, Stefanie C.</creator><creator>Richter, Antje M.</creator><creator>Fuhrmann, Liesa</creator><creator>El-Nikhely, Nefertiti</creator><creator>Seeger, Werner</creator><creator>Savai, Rajkumar</creator><creator>Dammann, Reinhard H.</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20141104</creationdate><title>ABCB4 is frequently epigenetically silenced in human cancers and inhibits tumor growth</title><author>Kiehl, Steffen ; Herkt, Stefanie C. ; Richter, Antje M. ; Fuhrmann, Liesa ; El-Nikhely, Nefertiti ; Seeger, Werner ; Savai, Rajkumar ; Dammann, Reinhard H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-a582d0ebf40b03f7182052b57c76c659afe071e7a6bb1a596829d78a53643dc53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>13/106</topic><topic>13/109</topic><topic>14/1</topic><topic>14/105</topic><topic>38/22</topic><topic>38/39</topic><topic>38/77</topic><topic>38/90</topic><topic>45/88</topic><topic>5-aza-2'-deoxycytidine</topic><topic>631/208/176</topic><topic>692/699/67/68</topic><topic>Animals</topic><topic>ATP Binding Cassette Transporter, Sub-Family B - genetics</topic><topic>ATP Binding Cassette Transporter, Sub-Family B - metabolism</topic><topic>Breast cancer</topic><topic>Carcinogenesis</topic><topic>Cell Proliferation</topic><topic>CpG Islands</topic><topic>DNA Methylation</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Head & neck cancer</topic><topic>HEK293 Cells</topic><topic>HeLa Cells</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Inactivation</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Methylation</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>multidisciplinary</topic><topic>Science</topic><topic>Skin</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kiehl, Steffen</creatorcontrib><creatorcontrib>Herkt, Stefanie C.</creatorcontrib><creatorcontrib>Richter, Antje M.</creatorcontrib><creatorcontrib>Fuhrmann, Liesa</creatorcontrib><creatorcontrib>El-Nikhely, Nefertiti</creatorcontrib><creatorcontrib>Seeger, Werner</creatorcontrib><creatorcontrib>Savai, Rajkumar</creatorcontrib><creatorcontrib>Dammann, Reinhard H.</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>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>Science Database (Alumni Edition)</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 One Sustainability</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kiehl, Steffen</au><au>Herkt, Stefanie C.</au><au>Richter, Antje M.</au><au>Fuhrmann, Liesa</au><au>El-Nikhely, Nefertiti</au><au>Seeger, Werner</au><au>Savai, Rajkumar</au><au>Dammann, Reinhard H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ABCB4 is frequently epigenetically silenced in human cancers and inhibits tumor growth</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2014-11-04</date><risdate>2014</risdate><volume>4</volume><issue>1</issue><spage>6899</spage><pages>6899-</pages><artnum>6899</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Epigenetic silencing through promoter hypermethylation is an important hallmark for the inactivation of tumor-related genes in carcinogenesis. Here we identified the
ATP-binding cassette sub-family B member 4 (ABCB4)
as a novel epigenetically silenced target gene. We investigated the epigenetic regulation of
ABCB4
in 26 human lung, breast, skin, liver, head and neck cancer cells lines and in primary cancers by methylation and expression analysis. Hypermethylation of the
ABCB4
CpG island promoter occurred in 16 out of 26 (62%) human cancer cell lines. Aberrant methylation of
ABCB4
was also revealed in 39% of primary lung cancer and in 20% of head and neck cancer tissues. In 37% of primary lung cancer samples, ABCB4 expression was absent. For breast cancer a significant hypermethylation occurred in tumor tissues (41%) compared to matching normal samples (0%, p = 0.002). Silencing of
ABCB4
was reversed by 5-aza-2'-deoxycytidine and zebularine treatments leading to its reexpression in cancer cells. Overexpression of ABCB4 significantly suppressed colony formation and proliferation of lung cancer cells. Hypermethylation of
Abcb4
occurred also in murine cancer, but was not found in normal tissues. Our findings suggest that
ABCB4
is a frequently silenced gene in different cancers and it may act tumor suppressivly in lung cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25367630</pmid><doi>10.1038/srep06899</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2045-2322 |
| ispartof | Scientific reports, 2014-11, Vol.4 (1), p.6899, Article 6899 |
| issn | 2045-2322 2045-2322 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4219162 |
| source | MEDLINE; Nature Free; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Springer Nature OA Free Journals |
| subjects | 13/106 13/109 14/1 14/105 38/22 38/39 38/77 38/90 45/88 5-aza-2'-deoxycytidine 631/208/176 692/699/67/68 Animals ATP Binding Cassette Transporter, Sub-Family B - genetics ATP Binding Cassette Transporter, Sub-Family B - metabolism Breast cancer Carcinogenesis Cell Proliferation CpG Islands DNA Methylation Epigenesis, Genetic Epigenetics Gene Expression Regulation, Neoplastic Head & neck cancer HEK293 Cells HeLa Cells Humanities and Social Sciences Humans Inactivation Liver Liver cancer Lung cancer Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Methylation Mice Mice, Inbred C57BL multidisciplinary Science Skin Tumor cell lines Tumors |
| title | ABCB4 is frequently epigenetically silenced in human cancers and inhibits tumor growth |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-29T01%3A44%3A19IST&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=ABCB4%20is%20frequently%20epigenetically%20silenced%20in%20human%20cancers%20and%20inhibits%20tumor%20growth&rft.jtitle=Scientific%20reports&rft.au=Kiehl,%20Steffen&rft.date=2014-11-04&rft.volume=4&rft.issue=1&rft.spage=6899&rft.pages=6899-&rft.artnum=6899&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/srep06899&rft_dat=%3Cproquest_pubme%3E1898173098%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=1898173098&rft_id=info:pmid/25367630&rfr_iscdi=true |