ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway
Renal cell carcinoma (RCC), which is one of the most diagnosed urological malignancies worldwide, is usually associated with abnormality in both genetic and cellular processes. In the present study, through analyzing The Cancer Genome Atlas (TCGA) dataset, we screened out ERCC6L as a candidate gene...
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| Veröffentlicht in: | Cancer gene therapy 2019-09, Vol.26 (9-10), p.323-333 |
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| creator | Zhang, Gejun Yu, Zi Fu, Shui Lv, Chengcheng Dong, Qingzhuo Fu, Cheng Kong, Chuize Zeng, Yu |
| description | Renal cell carcinoma (RCC), which is one of the most diagnosed urological malignancies worldwide, is usually associated with abnormality in both genetic and cellular processes. In the present study, through analyzing The Cancer Genome Atlas (TCGA) dataset, we screened out ERCC6L as a candidate gene that is potentially related to the development of RCC based on its increased expression in ccRCC tissues compared with normal kidney tissues as well as its possible relevance to cancer prognosis. Evidence indicates that ERCC6L is an indispensable component of mammalian cell mitosis, while it fails to disclose the role of ERCC6L in tumorigenesis. By using RT-PCR, it was confirmed that the mRNA expression of ERCC6L was upregulated in RCC tissues as compared to normal controls in 28 pared samples. In addition, the immunohistochemistry study in a tissue microarray (TMA) containing 150 ccRCC samples showed that the staining score of ERCC6L was positively correlated with the Fuhrman grade of cancers. Next, when the expression of ERCC6L was lowered by specific shRNA, the cell viability was significantly inhibited in 786-O and Caki-1 cells, while the apoptosis was induced accordingly. At the same time, RCC cells those were transfected with shRNA targeting to ERCC6L grew significantly slower than parental cells in immunodeficient mice. These results consistently suggest that ERCC6L may play a role in regulating the cell viability of RCC both in vitro and in vivo. Further, gene expression microarray analysis followed by the validating western blot after knocking down ERCC6L expression in 786-O cells highlighted the involvement of MAPK signaling pathway in regulation of ERCC6L on cellular process of RCC. In conclusion, the present study suggests a likely promoting role of ERCC6L on the development of RCC. Thus, further study to explore the potential utility of ERCC6L as a novel therapeutic target of RCC is clearly needed. |
| doi_str_mv | 10.1038/s41417-018-0064-8 |
| format | Article |
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In the present study, through analyzing The Cancer Genome Atlas (TCGA) dataset, we screened out ERCC6L as a candidate gene that is potentially related to the development of RCC based on its increased expression in ccRCC tissues compared with normal kidney tissues as well as its possible relevance to cancer prognosis. Evidence indicates that ERCC6L is an indispensable component of mammalian cell mitosis, while it fails to disclose the role of ERCC6L in tumorigenesis. By using RT-PCR, it was confirmed that the mRNA expression of ERCC6L was upregulated in RCC tissues as compared to normal controls in 28 pared samples. In addition, the immunohistochemistry study in a tissue microarray (TMA) containing 150 ccRCC samples showed that the staining score of ERCC6L was positively correlated with the Fuhrman grade of cancers. Next, when the expression of ERCC6L was lowered by specific shRNA, the cell viability was significantly inhibited in 786-O and Caki-1 cells, while the apoptosis was induced accordingly. At the same time, RCC cells those were transfected with shRNA targeting to ERCC6L grew significantly slower than parental cells in immunodeficient mice. These results consistently suggest that ERCC6L may play a role in regulating the cell viability of RCC both in vitro and in vivo. Further, gene expression microarray analysis followed by the validating western blot after knocking down ERCC6L expression in 786-O cells highlighted the involvement of MAPK signaling pathway in regulation of ERCC6L on cellular process of RCC. In conclusion, the present study suggests a likely promoting role of ERCC6L on the development of RCC. Thus, further study to explore the potential utility of ERCC6L as a novel therapeutic target of RCC is clearly needed.</description><identifier>ISSN: 0929-1903</identifier><identifier>EISSN: 1476-5500</identifier><identifier>DOI: 10.1038/s41417-018-0064-8</identifier><identifier>PMID: 30459398</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>13/2 ; 13/31 ; 13/51 ; 13/89 ; 38/61 ; 38/77 ; 42/35 ; 42/47 ; 631/61/51/2053 ; 631/67/589/1588 ; 631/80 ; 64/60 ; Animals ; Apoptosis ; Apoptosis - genetics ; Biomarkers ; Biomedicine ; Carcinogenesis ; Carcinoma, Renal cell ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - mortality ; Carcinoma, Renal Cell - pathology ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Cell viability ; Development and progression ; Disease Models, Animal ; DNA Helicases - genetics ; DNA Helicases - metabolism ; DNA microarrays ; Female ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Gene Therapy ; Genetic aspects ; Genomes ; Health aspects ; Heterografts ; Humans ; Identification and classification ; Immunodeficiency ; Immunohistochemistry ; Kidney cancer ; Kidney Neoplasms - genetics ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - mortality ; Kidney Neoplasms - pathology ; MAP kinase ; MAP Kinase Signaling System ; Medical prognosis ; Mice ; Mitogen-activated protein kinases ; Mitosis ; Oncogenes ; Physiological aspects ; Polymerase chain reaction ; Prognosis ; Renal cell carcinoma ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal transduction ; Therapeutic applications ; Therapeutic targets ; Tumorigenesis ; Urological cancer</subject><ispartof>Cancer gene therapy, 2019-09, Vol.26 (9-10), p.323-333</ispartof><rights>Springer Nature America, Inc. 2018. corrected publication 2022</rights><rights>COPYRIGHT 2019 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2019</rights><rights>Springer Nature America, Inc. 2018. corrected publication 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-c5653e0659c66ccc28671e9a6119542c6cb641552da9b979f9c7ecbd161aa52f3</citedby><cites>FETCH-LOGICAL-c498t-c5653e0659c66ccc28671e9a6119542c6cb641552da9b979f9c7ecbd161aa52f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41417-018-0064-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41417-018-0064-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30459398$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Gejun</creatorcontrib><creatorcontrib>Yu, Zi</creatorcontrib><creatorcontrib>Fu, Shui</creatorcontrib><creatorcontrib>Lv, Chengcheng</creatorcontrib><creatorcontrib>Dong, Qingzhuo</creatorcontrib><creatorcontrib>Fu, Cheng</creatorcontrib><creatorcontrib>Kong, Chuize</creatorcontrib><creatorcontrib>Zeng, Yu</creatorcontrib><title>ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway</title><title>Cancer gene therapy</title><addtitle>Cancer Gene Ther</addtitle><addtitle>Cancer Gene Ther</addtitle><description>Renal cell carcinoma (RCC), which is one of the most diagnosed urological malignancies worldwide, is usually associated with abnormality in both genetic and cellular processes. In the present study, through analyzing The Cancer Genome Atlas (TCGA) dataset, we screened out ERCC6L as a candidate gene that is potentially related to the development of RCC based on its increased expression in ccRCC tissues compared with normal kidney tissues as well as its possible relevance to cancer prognosis. Evidence indicates that ERCC6L is an indispensable component of mammalian cell mitosis, while it fails to disclose the role of ERCC6L in tumorigenesis. By using RT-PCR, it was confirmed that the mRNA expression of ERCC6L was upregulated in RCC tissues as compared to normal controls in 28 pared samples. In addition, the immunohistochemistry study in a tissue microarray (TMA) containing 150 ccRCC samples showed that the staining score of ERCC6L was positively correlated with the Fuhrman grade of cancers. Next, when the expression of ERCC6L was lowered by specific shRNA, the cell viability was significantly inhibited in 786-O and Caki-1 cells, while the apoptosis was induced accordingly. At the same time, RCC cells those were transfected with shRNA targeting to ERCC6L grew significantly slower than parental cells in immunodeficient mice. These results consistently suggest that ERCC6L may play a role in regulating the cell viability of RCC both in vitro and in vivo. Further, gene expression microarray analysis followed by the validating western blot after knocking down ERCC6L expression in 786-O cells highlighted the involvement of MAPK signaling pathway in regulation of ERCC6L on cellular process of RCC. In conclusion, the present study suggests a likely promoting role of ERCC6L on the development of RCC. Thus, further study to explore the potential utility of ERCC6L as a novel therapeutic target of RCC is clearly needed.</description><subject>13/2</subject><subject>13/31</subject><subject>13/51</subject><subject>13/89</subject><subject>38/61</subject><subject>38/77</subject><subject>42/35</subject><subject>42/47</subject><subject>631/61/51/2053</subject><subject>631/67/589/1588</subject><subject>631/80</subject><subject>64/60</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biomarkers</subject><subject>Biomedicine</subject><subject>Carcinogenesis</subject><subject>Carcinoma, Renal cell</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Carcinoma, Renal Cell - mortality</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Survival</subject><subject>Cell viability</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>DNA Helicases - genetics</subject><subject>DNA Helicases - metabolism</subject><subject>DNA microarrays</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Gene Therapy</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Identification and classification</subject><subject>Immunodeficiency</subject><subject>Immunohistochemistry</subject><subject>Kidney cancer</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - mortality</subject><subject>Kidney Neoplasms - pathology</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System</subject><subject>Medical prognosis</subject><subject>Mice</subject><subject>Mitogen-activated protein kinases</subject><subject>Mitosis</subject><subject>Oncogenes</subject><subject>Physiological aspects</subject><subject>Polymerase chain reaction</subject><subject>Prognosis</subject><subject>Renal cell carcinoma</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal transduction</subject><subject>Therapeutic applications</subject><subject>Therapeutic targets</subject><subject>Tumorigenesis</subject><subject>Urological cancer</subject><issn>0929-1903</issn><issn>1476-5500</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kl2L1DAUhoso7rj6A7yRgCDedE2aJm0uh2H9wBFF9LqcpmmbJU3GJJ1lfpt_zpSuuisqgYTkPO_5IG-WPSX4gmBavwolKUmVY1LnGPMyr-9lG1JWPGcM4_vZBotC5ERgepY9CuEK4xSs6MPsjOKSCSrqTfb98vNux_cojhCRDmg-5F4Ns4GoOqQtGvUwosFDp5DrkVcWDJLKpA281NZNgJQdwUoV1vejhlYbHU-L-qijdwhshw7eTS4mKM6T8ymju47jihwdOqSQjRqMOaVOvJtT0cl1SxvaDujD9tN7FPSQipvlfoA4XsPpcfagBxPUk5vzPPv6-vLL7m2-__jm3W67z2Up6phLxhlVmDMhOZdSFjWviBLACRGsLCSXLS8JY0UHohWV6IWslGw7wgkAK3p6nr1c86Yhvs0qxGbSYRkWrHJzaApCOWNlTcuEPv8DvXKzT30niheUCFFR-l-qEIQWlFe3cg1gVKNt76IHuZRutkyImqTPx4m6-AuVVqcmLZ1VvU7vdwQvbglGBSaOwZk5amfDXZCsoPQuBK_65uD1BP7UENws_mtW_zXJf83iv6ZOmmc3k83tpLpfip-GS0CxAiGF7KD879H_nfUHmNjk2A</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Zhang, Gejun</creator><creator>Yu, Zi</creator><creator>Fu, Shui</creator><creator>Lv, Chengcheng</creator><creator>Dong, Qingzhuo</creator><creator>Fu, Cheng</creator><creator>Kong, Chuize</creator><creator>Zeng, Yu</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</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>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>20190901</creationdate><title>ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway</title><author>Zhang, Gejun ; Yu, Zi ; Fu, Shui ; Lv, Chengcheng ; Dong, Qingzhuo ; Fu, Cheng ; Kong, Chuize ; Zeng, Yu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-c5653e0659c66ccc28671e9a6119542c6cb641552da9b979f9c7ecbd161aa52f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13/2</topic><topic>13/31</topic><topic>13/51</topic><topic>13/89</topic><topic>38/61</topic><topic>38/77</topic><topic>42/35</topic><topic>42/47</topic><topic>631/61/51/2053</topic><topic>631/67/589/1588</topic><topic>631/80</topic><topic>64/60</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biomarkers</topic><topic>Biomedicine</topic><topic>Carcinogenesis</topic><topic>Carcinoma, Renal cell</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Carcinoma, Renal Cell - mortality</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Survival</topic><topic>Cell viability</topic><topic>Development and progression</topic><topic>Disease Models, Animal</topic><topic>DNA Helicases - genetics</topic><topic>DNA Helicases - metabolism</topic><topic>DNA microarrays</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Gene Therapy</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Health aspects</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Identification and classification</topic><topic>Immunodeficiency</topic><topic>Immunohistochemistry</topic><topic>Kidney cancer</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - mortality</topic><topic>Kidney Neoplasms - pathology</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System</topic><topic>Medical prognosis</topic><topic>Mice</topic><topic>Mitogen-activated protein kinases</topic><topic>Mitosis</topic><topic>Oncogenes</topic><topic>Physiological aspects</topic><topic>Polymerase chain reaction</topic><topic>Prognosis</topic><topic>Renal cell carcinoma</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal transduction</topic><topic>Therapeutic applications</topic><topic>Therapeutic targets</topic><topic>Tumorigenesis</topic><topic>Urological cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Gejun</creatorcontrib><creatorcontrib>Yu, Zi</creatorcontrib><creatorcontrib>Fu, Shui</creatorcontrib><creatorcontrib>Lv, Chengcheng</creatorcontrib><creatorcontrib>Dong, Qingzhuo</creatorcontrib><creatorcontrib>Fu, Cheng</creatorcontrib><creatorcontrib>Kong, Chuize</creatorcontrib><creatorcontrib>Zeng, Yu</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</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>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</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>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Gejun</au><au>Yu, Zi</au><au>Fu, Shui</au><au>Lv, Chengcheng</au><au>Dong, Qingzhuo</au><au>Fu, Cheng</au><au>Kong, Chuize</au><au>Zeng, Yu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway</atitle><jtitle>Cancer gene therapy</jtitle><stitle>Cancer Gene Ther</stitle><addtitle>Cancer Gene Ther</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>26</volume><issue>9-10</issue><spage>323</spage><epage>333</epage><pages>323-333</pages><issn>0929-1903</issn><eissn>1476-5500</eissn><abstract>Renal cell carcinoma (RCC), which is one of the most diagnosed urological malignancies worldwide, is usually associated with abnormality in both genetic and cellular processes. In the present study, through analyzing The Cancer Genome Atlas (TCGA) dataset, we screened out ERCC6L as a candidate gene that is potentially related to the development of RCC based on its increased expression in ccRCC tissues compared with normal kidney tissues as well as its possible relevance to cancer prognosis. Evidence indicates that ERCC6L is an indispensable component of mammalian cell mitosis, while it fails to disclose the role of ERCC6L in tumorigenesis. By using RT-PCR, it was confirmed that the mRNA expression of ERCC6L was upregulated in RCC tissues as compared to normal controls in 28 pared samples. In addition, the immunohistochemistry study in a tissue microarray (TMA) containing 150 ccRCC samples showed that the staining score of ERCC6L was positively correlated with the Fuhrman grade of cancers. Next, when the expression of ERCC6L was lowered by specific shRNA, the cell viability was significantly inhibited in 786-O and Caki-1 cells, while the apoptosis was induced accordingly. At the same time, RCC cells those were transfected with shRNA targeting to ERCC6L grew significantly slower than parental cells in immunodeficient mice. These results consistently suggest that ERCC6L may play a role in regulating the cell viability of RCC both in vitro and in vivo. Further, gene expression microarray analysis followed by the validating western blot after knocking down ERCC6L expression in 786-O cells highlighted the involvement of MAPK signaling pathway in regulation of ERCC6L on cellular process of RCC. In conclusion, the present study suggests a likely promoting role of ERCC6L on the development of RCC. Thus, further study to explore the potential utility of ERCC6L as a novel therapeutic target of RCC is clearly needed.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>30459398</pmid><doi>10.1038/s41417-018-0064-8</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0929-1903 |
| ispartof | Cancer gene therapy, 2019-09, Vol.26 (9-10), p.323-333 |
| issn | 0929-1903 1476-5500 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2136554834 |
| source | MEDLINE; Springer Online Journals |
| subjects | 13/2 13/31 13/51 13/89 38/61 38/77 42/35 42/47 631/61/51/2053 631/67/589/1588 631/80 64/60 Animals Apoptosis Apoptosis - genetics Biomarkers Biomedicine Carcinogenesis Carcinoma, Renal cell Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Carcinoma, Renal Cell - mortality Carcinoma, Renal Cell - pathology Cell Line, Tumor Cell Proliferation Cell Survival Cell viability Development and progression Disease Models, Animal DNA Helicases - genetics DNA Helicases - metabolism DNA microarrays Female Gene Expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Gene Therapy Genetic aspects Genomes Health aspects Heterografts Humans Identification and classification Immunodeficiency Immunohistochemistry Kidney cancer Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - mortality Kidney Neoplasms - pathology MAP kinase MAP Kinase Signaling System Medical prognosis Mice Mitogen-activated protein kinases Mitosis Oncogenes Physiological aspects Polymerase chain reaction Prognosis Renal cell carcinoma RNA, Messenger - genetics RNA, Messenger - metabolism Signal transduction Therapeutic applications Therapeutic targets Tumorigenesis Urological cancer |
| title | ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T17%3A34%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ERCC6L%20that%20is%20up-regulated%20in%20high%20grade%20of%20renal%20cell%20carcinoma%20enhances%20cell%20viability%20in%20vitro%20and%20promotes%20tumor%20growth%20in%20vivo%20potentially%20through%20modulating%20MAPK%20signalling%20pathway&rft.jtitle=Cancer%20gene%20therapy&rft.au=Zhang,%20Gejun&rft.date=2019-09-01&rft.volume=26&rft.issue=9-10&rft.spage=323&rft.epage=333&rft.pages=323-333&rft.issn=0929-1903&rft.eissn=1476-5500&rft_id=info:doi/10.1038/s41417-018-0064-8&rft_dat=%3Cgale_proqu%3EA599811410%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2291323674&rft_id=info:pmid/30459398&rft_galeid=A599811410&rfr_iscdi=true |