Knockdown of ZEB1 , a master epithelial-to-mesenchymal transition (EMT) gene, suppresses anchorage-independent cell growth of lung cancer cells
Abstract We found that among four master epithelial-to-mesenchymal transition (EMT)-inducing genes ( ZEB1 , SIP1 , Snail , and Slug ) ZEB1 expression was most significantly correlated with the mesenchymal phenotype (high Vimentin and low E-cadherin expression) in non-small cell lung cancer (NSCLC) c...
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| Veröffentlicht in: | Cancer letters 2010-10, Vol.296 (2), p.216-224 |
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| creator | Takeyama, Yoshihiro Sato, Mitsuo Horio, Mihoko Hase, Tetsunari Yoshida, Kenya Yokoyama, Toshihiko Nakashima, Harunori Hashimoto, Naozumi Sekido, Yoshitaka Gazdar, Adi F Minna, John D Kondo, Masashi Hasegawa, Yoshinori |
| description | Abstract We found that among four master epithelial-to-mesenchymal transition (EMT)-inducing genes ( ZEB1 , SIP1 , Snail , and Slug ) ZEB1 expression was most significantly correlated with the mesenchymal phenotype (high Vimentin and low E-cadherin expression) in non-small cell lung cancer (NSCLC) cell lines and tumors. Furthermore, ZEB1 knockdown with RNA interference in three NSCLC cell lines with high ZEB1 expression suppressed to varying degrees mass culture growth and liquid colony formation but in all cases dramatically suppressed soft agar colony formation. In addition, ZEB1 knockdown induced apoptosis in one of the three lines, indicating that the growth inhibitory effects of ZEB1 knockdown occurs in part through the activation of the apoptosis pathway. These results suggest that inhibiting ZEB1 function may be an attractive target for NSCLC therapeutic development. |
| doi_str_mv | 10.1016/j.canlet.2010.04.008 |
| format | Article |
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Furthermore, ZEB1 knockdown with RNA interference in three NSCLC cell lines with high ZEB1 expression suppressed to varying degrees mass culture growth and liquid colony formation but in all cases dramatically suppressed soft agar colony formation. In addition, ZEB1 knockdown induced apoptosis in one of the three lines, indicating that the growth inhibitory effects of ZEB1 knockdown occurs in part through the activation of the apoptosis pathway. These results suggest that inhibiting ZEB1 function may be an attractive target for NSCLC therapeutic development.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2010.04.008</identifier><identifier>PMID: 20452118</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Anchorage-independent growth ; Apoptosis ; Apoptosis - genetics ; Breast cancer ; Cadherins - genetics ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Division ; Cell Line, Tumor ; EMT ; Epidermal growth factor receptor ; Epithelial Cells - pathology ; Gene Knockdown Techniques ; Genes ; Genotype & phenotype ; Hematology, Oncology and Palliative Medicine ; Homeodomain Proteins - genetics ; Humans ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Medical prognosis ; Mesoderm - pathology ; Mesothelioma - genetics ; Mesothelioma - pathology ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; Mutation ; Proteins ; Receptor, Epidermal Growth Factor - genetics ; RNA interference ; RNA, Small Interfering - genetics ; Transcription factors ; Transcription Factors - genetics ; Values ; Vimentin - genetics ; Zinc Finger E-box-Binding Homeobox 1</subject><ispartof>Cancer letters, 2010-10, Vol.296 (2), p.216-224</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2010 Elsevier Ireland Ltd</rights><rights>2010 Elsevier Ireland Ltd. All rights reserved.</rights><rights>Copyright Elsevier Limited Oct 28, 2010</rights><rights>2010 Elsevier Ireland Ltd. All rights reserved. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c611t-8bf1670d592df25d38fea252b97478b4c38db2ecef28f95ad24d979ceb07dec13</citedby><cites>FETCH-LOGICAL-c611t-8bf1670d592df25d38fea252b97478b4c38db2ecef28f95ad24d979ceb07dec13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2010.04.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,777,781,882,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20452118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takeyama, Yoshihiro</creatorcontrib><creatorcontrib>Sato, Mitsuo</creatorcontrib><creatorcontrib>Horio, Mihoko</creatorcontrib><creatorcontrib>Hase, Tetsunari</creatorcontrib><creatorcontrib>Yoshida, Kenya</creatorcontrib><creatorcontrib>Yokoyama, Toshihiko</creatorcontrib><creatorcontrib>Nakashima, Harunori</creatorcontrib><creatorcontrib>Hashimoto, Naozumi</creatorcontrib><creatorcontrib>Sekido, Yoshitaka</creatorcontrib><creatorcontrib>Gazdar, Adi F</creatorcontrib><creatorcontrib>Minna, John D</creatorcontrib><creatorcontrib>Kondo, Masashi</creatorcontrib><creatorcontrib>Hasegawa, Yoshinori</creatorcontrib><title>Knockdown of ZEB1 , a master epithelial-to-mesenchymal transition (EMT) gene, suppresses anchorage-independent cell growth of lung cancer cells</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Abstract We found that among four master epithelial-to-mesenchymal transition (EMT)-inducing genes ( ZEB1 , SIP1 , Snail , and Slug ) ZEB1 expression was most significantly correlated with the mesenchymal phenotype (high Vimentin and low E-cadherin expression) in non-small cell lung cancer (NSCLC) cell lines and tumors. Furthermore, ZEB1 knockdown with RNA interference in three NSCLC cell lines with high ZEB1 expression suppressed to varying degrees mass culture growth and liquid colony formation but in all cases dramatically suppressed soft agar colony formation. In addition, ZEB1 knockdown induced apoptosis in one of the three lines, indicating that the growth inhibitory effects of ZEB1 knockdown occurs in part through the activation of the apoptosis pathway. These results suggest that inhibiting ZEB1 function may be an attractive target for NSCLC therapeutic development.</description><subject>Anchorage-independent growth</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Breast cancer</subject><subject>Cadherins - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Division</subject><subject>Cell Line, Tumor</subject><subject>EMT</subject><subject>Epidermal growth factor receptor</subject><subject>Epithelial Cells - pathology</subject><subject>Gene Knockdown Techniques</subject><subject>Genes</subject><subject>Genotype & phenotype</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Homeodomain Proteins - genetics</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Medical prognosis</subject><subject>Mesoderm - pathology</subject><subject>Mesothelioma - genetics</subject><subject>Mesothelioma - pathology</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Mutation</subject><subject>Proteins</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>RNA interference</subject><subject>RNA, Small Interfering - genetics</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><subject>Values</subject><subject>Vimentin - genetics</subject><subject>Zinc Finger E-box-Binding Homeobox 1</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUk1v1DAUjBCILoV_gJAlDoDULLZjb5wLElTLhyjiQLlwsRz7Zddbxw520mp_BX8ZR1ta6IWLLfnNm3njeUXxlOAlwWT1erfUyjsYlxTnJ8yWGIt7xYKImpZ1I_D9YoErzMpKVPyoeJTSDmPMWc0fFkcUM04JEYvi12cf9IUJVx6FDv1YvyPoBCnUqzRCRDDYcQvOKleOoewhgdfbfa8cGqPyyY42ePRy_eX8FdqAhxOUpmGIkBIkpDI0RLWB0noDA-TDj0iDc2gTw9W4nQXd5Dco-9BZbC6lx8WDTrkET67v4-L7-_X56cfy7OuHT6dvz0q9ImQsRduRVY0Nb6jpKDeV6EBRTtumZrVoma6EaSlo6KjoGq4MZaapGw0trg1oUh0Xbw68w9T2YHSeLSonh2h7FfcyKCv_rXi7lZtwKStCsKA8E7y4Jojh5wRplL1NswXlIUxJ1kw0lDWUZuTzO8hdmKLP7iTheIX5qiYso9gBpWNIKUJ3MwvBcg5c7uQhcDkHLjGTOfDc9uxvHzdNfxK-NQr5Ny8tRJm0zTGCsRH0KE2w_1O4S6Cd9VYrdwF7SLdeZKISy2_z0s07R_K6UUJx9Ru0QdWE</recordid><startdate>20101028</startdate><enddate>20101028</enddate><creator>Takeyama, Yoshihiro</creator><creator>Sato, Mitsuo</creator><creator>Horio, Mihoko</creator><creator>Hase, Tetsunari</creator><creator>Yoshida, Kenya</creator><creator>Yokoyama, Toshihiko</creator><creator>Nakashima, Harunori</creator><creator>Hashimoto, Naozumi</creator><creator>Sekido, Yoshitaka</creator><creator>Gazdar, Adi F</creator><creator>Minna, John D</creator><creator>Kondo, Masashi</creator><creator>Hasegawa, Yoshinori</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Limited</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20101028</creationdate><title>Knockdown of ZEB1 , a master epithelial-to-mesenchymal transition (EMT) gene, suppresses anchorage-independent cell growth of lung cancer cells</title><author>Takeyama, Yoshihiro ; Sato, Mitsuo ; Horio, Mihoko ; Hase, Tetsunari ; Yoshida, Kenya ; Yokoyama, Toshihiko ; Nakashima, Harunori ; Hashimoto, Naozumi ; Sekido, Yoshitaka ; Gazdar, Adi F ; Minna, John D ; Kondo, Masashi ; Hasegawa, Yoshinori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c611t-8bf1670d592df25d38fea252b97478b4c38db2ecef28f95ad24d979ceb07dec13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Anchorage-independent growth</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Breast cancer</topic><topic>Cadherins - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Division</topic><topic>Cell Line, Tumor</topic><topic>EMT</topic><topic>Epidermal growth factor receptor</topic><topic>Epithelial Cells - pathology</topic><topic>Gene Knockdown Techniques</topic><topic>Genes</topic><topic>Genotype & phenotype</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Homeodomain Proteins - genetics</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Medical prognosis</topic><topic>Mesoderm - pathology</topic><topic>Mesothelioma - genetics</topic><topic>Mesothelioma - pathology</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>Mutation</topic><topic>Proteins</topic><topic>Receptor, Epidermal Growth Factor - genetics</topic><topic>RNA interference</topic><topic>RNA, Small Interfering - genetics</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><topic>Values</topic><topic>Vimentin - genetics</topic><topic>Zinc Finger E-box-Binding Homeobox 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takeyama, Yoshihiro</creatorcontrib><creatorcontrib>Sato, Mitsuo</creatorcontrib><creatorcontrib>Horio, Mihoko</creatorcontrib><creatorcontrib>Hase, Tetsunari</creatorcontrib><creatorcontrib>Yoshida, Kenya</creatorcontrib><creatorcontrib>Yokoyama, Toshihiko</creatorcontrib><creatorcontrib>Nakashima, Harunori</creatorcontrib><creatorcontrib>Hashimoto, Naozumi</creatorcontrib><creatorcontrib>Sekido, Yoshitaka</creatorcontrib><creatorcontrib>Gazdar, Adi F</creatorcontrib><creatorcontrib>Minna, John D</creatorcontrib><creatorcontrib>Kondo, Masashi</creatorcontrib><creatorcontrib>Hasegawa, Yoshinori</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takeyama, Yoshihiro</au><au>Sato, Mitsuo</au><au>Horio, Mihoko</au><au>Hase, Tetsunari</au><au>Yoshida, Kenya</au><au>Yokoyama, Toshihiko</au><au>Nakashima, Harunori</au><au>Hashimoto, Naozumi</au><au>Sekido, Yoshitaka</au><au>Gazdar, Adi F</au><au>Minna, John D</au><au>Kondo, Masashi</au><au>Hasegawa, Yoshinori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockdown of ZEB1 , a master epithelial-to-mesenchymal transition (EMT) gene, suppresses anchorage-independent cell growth of lung cancer cells</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2010-10-28</date><risdate>2010</risdate><volume>296</volume><issue>2</issue><spage>216</spage><epage>224</epage><pages>216-224</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Abstract We found that among four master epithelial-to-mesenchymal transition (EMT)-inducing genes ( ZEB1 , SIP1 , Snail , and Slug ) ZEB1 expression was most significantly correlated with the mesenchymal phenotype (high Vimentin and low E-cadherin expression) in non-small cell lung cancer (NSCLC) cell lines and tumors. Furthermore, ZEB1 knockdown with RNA interference in three NSCLC cell lines with high ZEB1 expression suppressed to varying degrees mass culture growth and liquid colony formation but in all cases dramatically suppressed soft agar colony formation. In addition, ZEB1 knockdown induced apoptosis in one of the three lines, indicating that the growth inhibitory effects of ZEB1 knockdown occurs in part through the activation of the apoptosis pathway. These results suggest that inhibiting ZEB1 function may be an attractive target for NSCLC therapeutic development.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>20452118</pmid><doi>10.1016/j.canlet.2010.04.008</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Cancer letters, 2010-10, Vol.296 (2), p.216-224 |
| issn | 0304-3835 1872-7980 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Anchorage-independent growth Apoptosis Apoptosis - genetics Breast cancer Cadherins - genetics Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Cell Division Cell Line, Tumor EMT Epidermal growth factor receptor Epithelial Cells - pathology Gene Knockdown Techniques Genes Genotype & phenotype Hematology, Oncology and Palliative Medicine Homeodomain Proteins - genetics Humans Lung cancer Lung Neoplasms - genetics Lung Neoplasms - pathology Medical prognosis Mesoderm - pathology Mesothelioma - genetics Mesothelioma - pathology MicroRNA MicroRNAs MicroRNAs - genetics Mutation Proteins Receptor, Epidermal Growth Factor - genetics RNA interference RNA, Small Interfering - genetics Transcription factors Transcription Factors - genetics Values Vimentin - genetics Zinc Finger E-box-Binding Homeobox 1 |
| title | Knockdown of ZEB1 , a master epithelial-to-mesenchymal transition (EMT) gene, suppresses anchorage-independent cell growth of lung cancer cells |
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