TBL1XR1 is involved in c-Met-mediated tumorigenesis of human nonsmall cell lung cancer
Nonsmall cell lung carcinoma (NSCLC) contributes to the highest number of cancer deaths globally. Metastases and chemoresistance are two major confounders to the treatment efficacy in NSCLC. Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) has been associated with high rates of metastases in brea...
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| Veröffentlicht in: | Cancer gene therapy 2020-04, Vol.27 (3-4), p.136-146 |
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| container_title | Cancer gene therapy |
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| creator | Zhang, Tiewa Liu, Cheng Yu, Yan Geng, Jianxiong Meng, Qingwei Xu, Shanqi Zhou, Fengrui Chen, Yingying Jin, Shi Shen, Jing Pan, Bo Meng, Fanling Liu, Fang |
| description | Nonsmall cell lung carcinoma (NSCLC) contributes to the highest number of cancer deaths globally. Metastases and chemoresistance are two major confounders to the treatment efficacy in NSCLC. Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) has been associated with high rates of metastases in breast, gastric, and stomach cancers. However, the role of TBL1XR1 in lung cancers remains underexplored. We selected matched and cancerous lung tissues to establish the upregulation of TBL1XR1. Using in vitro assays, we assessed the influence of TBL1XR1 on various cancer phenotypes, namely cell proliferation, chemoresistance, invasion, and metastases in a CRISPR-Cas9-mediated knock out model (A549 cells), and H460 cell lines overexpressing TBL1XR1. We found that TBL1XR1 is overexpressed in NSCLC tissue and patient sera in comparison to paired adjacent normal tissue. Overexpression of TBL1XR1 in NSCLC cell lines mediates cell survival, proliferation, and metastases. TBL1XR1 was found to regulate MEK and Akt pathways through their master regulator c-Met. We observed that activation of c-Met is downregulated in the absence of TBL1XR1. Our study strengthens the contention that TBL1XR1 is a biomarker for prognosis of NSCLC. It may also be considered as an adjunct or core therapeutic target to overcome cisplatin resistance in lung cancers. |
| doi_str_mv | 10.1038/s41417-019-0111-0 |
| format | Article |
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Metastases and chemoresistance are two major confounders to the treatment efficacy in NSCLC. Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) has been associated with high rates of metastases in breast, gastric, and stomach cancers. However, the role of TBL1XR1 in lung cancers remains underexplored. We selected matched and cancerous lung tissues to establish the upregulation of TBL1XR1. Using in vitro assays, we assessed the influence of TBL1XR1 on various cancer phenotypes, namely cell proliferation, chemoresistance, invasion, and metastases in a CRISPR-Cas9-mediated knock out model (A549 cells), and H460 cell lines overexpressing TBL1XR1. We found that TBL1XR1 is overexpressed in NSCLC tissue and patient sera in comparison to paired adjacent normal tissue. Overexpression of TBL1XR1 in NSCLC cell lines mediates cell survival, proliferation, and metastases. TBL1XR1 was found to regulate MEK and Akt pathways through their master regulator c-Met. We observed that activation of c-Met is downregulated in the absence of TBL1XR1. Our study strengthens the contention that TBL1XR1 is a biomarker for prognosis of NSCLC. It may also be considered as an adjunct or core therapeutic target to overcome cisplatin resistance in lung cancers.</description><identifier>ISSN: 0929-1903</identifier><identifier>EISSN: 1476-5500</identifier><identifier>DOI: 10.1038/s41417-019-0111-0</identifier><identifier>PMID: 31243347</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject><![CDATA[42/109 ; 42/41 ; 631/67/1612/1350 ; 631/67/395 ; 82/80 ; A549 Cells ; Adult ; Aged ; AKT protein ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Biotechnology & Applied Microbiology ; Breast ; Carcinogenesis - genetics ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Carcinoma, Non-Small-Cell Lung - therapy ; Care and treatment ; Cell proliferation ; Cell Proliferation - genetics ; Cell survival ; Cell Survival - genetics ; Chemoresistance ; Chemotherapy, Adjuvant - methods ; Cisplatin ; Cisplatin - pharmacology ; Cisplatin - therapeutic use ; CRISPR ; Development and progression ; Drug Resistance, Neoplasm - genetics ; Female ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Gene Knockout Techniques ; Gene Therapy ; Genetic aspects ; Genetic regulation ; Genetics & Heredity ; Health aspects ; Humans ; Life Sciences & Biomedicine ; Lung - pathology ; Lung - surgery ; Lung cancer ; Lung cancer, Non-small cell ; Lung carcinoma ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Lung Neoplasms - therapy ; Male ; MAP Kinase Signaling System - genetics ; Medical prognosis ; Medicine, Research & Experimental ; Metastases ; Metastasis ; Middle Aged ; Non-small cell lung carcinoma ; Oncology ; Phenotypes ; Pneumonectomy ; Prognosis ; Proto-Oncogene Proteins c-met - metabolism ; Receptors, Cytoplasmic and Nuclear - genetics ; Receptors, Cytoplasmic and Nuclear - metabolism ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Research & Experimental Medicine ; Science & Technology ; Therapeutic applications ; Transducin ; Treatment Outcome ; Tumorigenesis ; Up-Regulation]]></subject><ispartof>Cancer gene therapy, 2020-04, Vol.27 (3-4), p.136-146</ispartof><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. 2019</rights><rights>COPYRIGHT 2020 Nature Publishing Group</rights><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. 2019.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>15</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000527373700004</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c470t-85408a463506eb4096c0bb57a4de0c997ce2c89b935cbb08cb3bf241d81eec243</citedby><cites>FETCH-LOGICAL-c470t-85408a463506eb4096c0bb57a4de0c997ce2c89b935cbb08cb3bf241d81eec243</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31243347$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Tiewa</creatorcontrib><creatorcontrib>Liu, Cheng</creatorcontrib><creatorcontrib>Yu, Yan</creatorcontrib><creatorcontrib>Geng, Jianxiong</creatorcontrib><creatorcontrib>Meng, Qingwei</creatorcontrib><creatorcontrib>Xu, Shanqi</creatorcontrib><creatorcontrib>Zhou, Fengrui</creatorcontrib><creatorcontrib>Chen, Yingying</creatorcontrib><creatorcontrib>Jin, Shi</creatorcontrib><creatorcontrib>Shen, Jing</creatorcontrib><creatorcontrib>Pan, Bo</creatorcontrib><creatorcontrib>Meng, Fanling</creatorcontrib><creatorcontrib>Liu, Fang</creatorcontrib><title>TBL1XR1 is involved in c-Met-mediated tumorigenesis of human nonsmall cell lung cancer</title><title>Cancer gene therapy</title><addtitle>Cancer Gene Ther</addtitle><addtitle>CANCER GENE THER</addtitle><addtitle>Cancer Gene Ther</addtitle><description>Nonsmall cell lung carcinoma (NSCLC) contributes to the highest number of cancer deaths globally. Metastases and chemoresistance are two major confounders to the treatment efficacy in NSCLC. Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) has been associated with high rates of metastases in breast, gastric, and stomach cancers. However, the role of TBL1XR1 in lung cancers remains underexplored. We selected matched and cancerous lung tissues to establish the upregulation of TBL1XR1. Using in vitro assays, we assessed the influence of TBL1XR1 on various cancer phenotypes, namely cell proliferation, chemoresistance, invasion, and metastases in a CRISPR-Cas9-mediated knock out model (A549 cells), and H460 cell lines overexpressing TBL1XR1. We found that TBL1XR1 is overexpressed in NSCLC tissue and patient sera in comparison to paired adjacent normal tissue. Overexpression of TBL1XR1 in NSCLC cell lines mediates cell survival, proliferation, and metastases. TBL1XR1 was found to regulate MEK and Akt pathways through their master regulator c-Met. We observed that activation of c-Met is downregulated in the absence of TBL1XR1. Our study strengthens the contention that TBL1XR1 is a biomarker for prognosis of NSCLC. It may also be considered as an adjunct or core therapeutic target to overcome cisplatin resistance in lung cancers.</description><subject>42/109</subject><subject>42/41</subject><subject>631/67/1612/1350</subject><subject>631/67/395</subject><subject>82/80</subject><subject>A549 Cells</subject><subject>Adult</subject><subject>Aged</subject><subject>AKT protein</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Biotechnology & Applied Microbiology</subject><subject>Breast</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Carcinoma, Non-Small-Cell Lung - therapy</subject><subject>Care and treatment</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell survival</subject><subject>Cell Survival - genetics</subject><subject>Chemoresistance</subject><subject>Chemotherapy, Adjuvant - methods</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Cisplatin - therapeutic use</subject><subject>CRISPR</subject><subject>Development and progression</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockout Techniques</subject><subject>Gene Therapy</subject><subject>Genetic aspects</subject><subject>Genetic regulation</subject><subject>Genetics & Heredity</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Life Sciences & Biomedicine</subject><subject>Lung - pathology</subject><subject>Lung - surgery</subject><subject>Lung cancer</subject><subject>Lung cancer, Non-small cell</subject><subject>Lung carcinoma</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Lung Neoplasms - therapy</subject><subject>Male</subject><subject>MAP Kinase Signaling System - genetics</subject><subject>Medical prognosis</subject><subject>Medicine, Research & Experimental</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Non-small cell lung carcinoma</subject><subject>Oncology</subject><subject>Phenotypes</subject><subject>Pneumonectomy</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins c-met - metabolism</subject><subject>Receptors, Cytoplasmic and Nuclear - genetics</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Research & Experimental Medicine</subject><subject>Science & Technology</subject><subject>Therapeutic applications</subject><subject>Transducin</subject><subject>Treatment Outcome</subject><subject>Tumorigenesis</subject><subject>Up-Regulation</subject><issn>0929-1903</issn><issn>1476-5500</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkV2L1TAQhoMo7nH1B3gjBUEE6Tpp0o9crge_4Iggq3gX0nR6TpY2WZt0xX_vlK67rihISDIkzzvMzMvYYw4nHETzMkoueZ0DV7Q5z-EO23BZV3lZAtxlG1CFyrkCccQexHgOQJ-1uM-OBC-kELLesC9nr3b86yeeuZg5fxmGS-woyGz-AVM-YudMopc0j2Fye_QYCQx9dphH4zMffBzNMGQW6Rhmv8-s8Ranh-xeb4aIj67uY_b5zeuz7bt89_Ht--3pLreyhpQ3pYTGyEqUUGErQVUW2rasjewQrFK1xcI2qlWitG0LjW1F2xeSdw1HtNTDMXu-5r2YwrcZY9Kji0sxxmOYoy4K2YiGl7Im9Okf6HmYJ0_V6UIoSiqlkjfU3gyone9DmoxdkurTquBSVWXDiTr5C0Wrw9HZ4LF39H5L8Ow3wQHNkA4xDHNyNMHbIF9BO4UYJ-z1xeRGM_3QHPRiul5N12S6XkzXQJonV53NLTl2rfjlMgEvVuA7tqGP1iF5dI0BQFnUghZFsIyg-X9665JZmtiG2SeSFqs0Eu73ON3M-N_l_wTXLdN4</recordid><startdate>20200401</startdate><enddate>20200401</enddate><creator>Zhang, Tiewa</creator><creator>Liu, Cheng</creator><creator>Yu, Yan</creator><creator>Geng, Jianxiong</creator><creator>Meng, Qingwei</creator><creator>Xu, Shanqi</creator><creator>Zhou, Fengrui</creator><creator>Chen, Yingying</creator><creator>Jin, Shi</creator><creator>Shen, Jing</creator><creator>Pan, Bo</creator><creator>Meng, Fanling</creator><creator>Liu, Fang</creator><general>Nature Publishing Group US</general><general>Springer Nature</general><general>Nature Publishing Group</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</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>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20200401</creationdate><title>TBL1XR1 is involved in c-Met-mediated tumorigenesis of human nonsmall cell lung cancer</title><author>Zhang, Tiewa ; Liu, Cheng ; Yu, Yan ; Geng, Jianxiong ; Meng, Qingwei ; Xu, Shanqi ; Zhou, Fengrui ; Chen, Yingying ; Jin, Shi ; Shen, Jing ; Pan, Bo ; Meng, Fanling ; Liu, Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-85408a463506eb4096c0bb57a4de0c997ce2c89b935cbb08cb3bf241d81eec243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>42/109</topic><topic>42/41</topic><topic>631/67/1612/1350</topic><topic>631/67/395</topic><topic>82/80</topic><topic>A549 Cells</topic><topic>Adult</topic><topic>Aged</topic><topic>AKT protein</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Biotechnology & Applied Microbiology</topic><topic>Breast</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Carcinoma, Non-Small-Cell Lung - therapy</topic><topic>Care and treatment</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell survival</topic><topic>Cell Survival - genetics</topic><topic>Chemoresistance</topic><topic>Chemotherapy, Adjuvant - methods</topic><topic>Cisplatin</topic><topic>Cisplatin - pharmacology</topic><topic>Cisplatin - therapeutic use</topic><topic>CRISPR</topic><topic>Development and progression</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockout Techniques</topic><topic>Gene Therapy</topic><topic>Genetic aspects</topic><topic>Genetic regulation</topic><topic>Genetics & Heredity</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Life Sciences & Biomedicine</topic><topic>Lung - 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Academic</collection><jtitle>Cancer gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Tiewa</au><au>Liu, Cheng</au><au>Yu, Yan</au><au>Geng, Jianxiong</au><au>Meng, Qingwei</au><au>Xu, Shanqi</au><au>Zhou, Fengrui</au><au>Chen, Yingying</au><au>Jin, Shi</au><au>Shen, Jing</au><au>Pan, Bo</au><au>Meng, Fanling</au><au>Liu, Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TBL1XR1 is involved in c-Met-mediated tumorigenesis of human nonsmall cell lung cancer</atitle><jtitle>Cancer gene therapy</jtitle><stitle>Cancer Gene Ther</stitle><stitle>CANCER GENE THER</stitle><addtitle>Cancer Gene Ther</addtitle><date>2020-04-01</date><risdate>2020</risdate><volume>27</volume><issue>3-4</issue><spage>136</spage><epage>146</epage><pages>136-146</pages><issn>0929-1903</issn><eissn>1476-5500</eissn><abstract>Nonsmall cell lung carcinoma (NSCLC) contributes to the highest number of cancer deaths globally. Metastases and chemoresistance are two major confounders to the treatment efficacy in NSCLC. Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) has been associated with high rates of metastases in breast, gastric, and stomach cancers. However, the role of TBL1XR1 in lung cancers remains underexplored. We selected matched and cancerous lung tissues to establish the upregulation of TBL1XR1. Using in vitro assays, we assessed the influence of TBL1XR1 on various cancer phenotypes, namely cell proliferation, chemoresistance, invasion, and metastases in a CRISPR-Cas9-mediated knock out model (A549 cells), and H460 cell lines overexpressing TBL1XR1. We found that TBL1XR1 is overexpressed in NSCLC tissue and patient sera in comparison to paired adjacent normal tissue. Overexpression of TBL1XR1 in NSCLC cell lines mediates cell survival, proliferation, and metastases. TBL1XR1 was found to regulate MEK and Akt pathways through their master regulator c-Met. We observed that activation of c-Met is downregulated in the absence of TBL1XR1. Our study strengthens the contention that TBL1XR1 is a biomarker for prognosis of NSCLC. It may also be considered as an adjunct or core therapeutic target to overcome cisplatin resistance in lung cancers.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>31243347</pmid><doi>10.1038/s41417-019-0111-0</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0929-1903 |
| ispartof | Cancer gene therapy, 2020-04, Vol.27 (3-4), p.136-146 |
| issn | 0929-1903 1476-5500 |
| language | eng |
| recordid | cdi_gale_infotracmisc_A621496581 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | 42/109 42/41 631/67/1612/1350 631/67/395 82/80 A549 Cells Adult Aged AKT protein Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Biomedical and Life Sciences Biomedicine Biotechnology & Applied Microbiology Breast Carcinogenesis - genetics Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Carcinoma, Non-Small-Cell Lung - therapy Care and treatment Cell proliferation Cell Proliferation - genetics Cell survival Cell Survival - genetics Chemoresistance Chemotherapy, Adjuvant - methods Cisplatin Cisplatin - pharmacology Cisplatin - therapeutic use CRISPR Development and progression Drug Resistance, Neoplasm - genetics Female Gene Expression Gene Expression Regulation, Neoplastic Gene Knockout Techniques Gene Therapy Genetic aspects Genetic regulation Genetics & Heredity Health aspects Humans Life Sciences & Biomedicine Lung - pathology Lung - surgery Lung cancer Lung cancer, Non-small cell Lung carcinoma Lung Neoplasms - genetics Lung Neoplasms - pathology Lung Neoplasms - therapy Male MAP Kinase Signaling System - genetics Medical prognosis Medicine, Research & Experimental Metastases Metastasis Middle Aged Non-small cell lung carcinoma Oncology Phenotypes Pneumonectomy Prognosis Proto-Oncogene Proteins c-met - metabolism Receptors, Cytoplasmic and Nuclear - genetics Receptors, Cytoplasmic and Nuclear - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism Research & Experimental Medicine Science & Technology Therapeutic applications Transducin Treatment Outcome Tumorigenesis Up-Regulation |
| title | TBL1XR1 is involved in c-Met-mediated tumorigenesis of human nonsmall cell lung cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-17T11%3A27%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TBL1XR1%20is%20involved%20in%20c-Met-mediated%20tumorigenesis%20of%20human%20nonsmall%20cell%20lung%20cancer&rft.jtitle=Cancer%20gene%20therapy&rft.au=Zhang,%20Tiewa&rft.date=2020-04-01&rft.volume=27&rft.issue=3-4&rft.spage=136&rft.epage=146&rft.pages=136-146&rft.issn=0929-1903&rft.eissn=1476-5500&rft_id=info:doi/10.1038/s41417-019-0111-0&rft_dat=%3Cgale_cross%3EA621496581%3C/gale_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2392414494&rft_id=info:pmid/31243347&rft_galeid=A621496581&rfr_iscdi=true |