Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway
Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear. RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed...
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| Veröffentlicht in: | Journal of experimental & clinical cancer research 2015-11, Vol.34 (135), p.135-135, Article 135 |
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| container_title | Journal of experimental & clinical cancer research |
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| creator | Zhou, Jianping Zhi, Xiaofei Wang, Linjun Wang, Weizhi Li, Zheng Tang, Jie Wang, Jiwei Zhang, Qun Xu, Zekuan |
| description | Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear.
RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay.
In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling.
We first found that Linc00152 could promote tumor growth through EGFR-mediated PI3K/AKT pathway which may serve as potential targets for therapy in the future. |
| doi_str_mv | 10.1186/s13046-015-0250-6 |
| format | Article |
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RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay.
In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling.
We first found that Linc00152 could promote tumor growth through EGFR-mediated PI3K/AKT pathway which may serve as potential targets for therapy in the future.</description><identifier>ISSN: 1756-9966</identifier><identifier>ISSN: 0392-9078</identifier><identifier>EISSN: 1756-9966</identifier><identifier>DOI: 10.1186/s13046-015-0250-6</identifier><identifier>PMID: 26538117</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Care and treatment ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cholecystokinin ; Complications and side effects ; Cytoplasm - metabolism ; Development and progression ; Disease Models, Animal ; Heterografts ; Humans ; Mice ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Receptor, Epidermal Growth Factor - metabolism ; RNA Transport ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction ; Stomach cancer ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Tumor Burden - genetics</subject><ispartof>Journal of experimental & clinical cancer research, 2015-11, Vol.34 (135), p.135-135, Article 135</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>Zhou et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c591t-abeeecbc3ba6d3eada4b9bee9b543dc2617ef93102e4c7cc87f749aa62ad17f83</citedby><cites>FETCH-LOGICAL-c591t-abeeecbc3ba6d3eada4b9bee9b543dc2617ef93102e4c7cc87f749aa62ad17f83</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/PMC4632266/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632266/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26538117$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Jianping</creatorcontrib><creatorcontrib>Zhi, Xiaofei</creatorcontrib><creatorcontrib>Wang, Linjun</creatorcontrib><creatorcontrib>Wang, Weizhi</creatorcontrib><creatorcontrib>Li, Zheng</creatorcontrib><creatorcontrib>Tang, Jie</creatorcontrib><creatorcontrib>Wang, Jiwei</creatorcontrib><creatorcontrib>Zhang, Qun</creatorcontrib><creatorcontrib>Xu, Zekuan</creatorcontrib><title>Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway</title><title>Journal of experimental & clinical cancer research</title><addtitle>J Exp Clin Cancer Res</addtitle><description>Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear.
RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay.
In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling.
We first found that Linc00152 could promote tumor growth through EGFR-mediated PI3K/AKT pathway which may serve as potential targets for therapy in the future.</description><subject>Animals</subject><subject>Care and treatment</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cholecystokinin</subject><subject>Complications and side effects</subject><subject>Cytoplasm - metabolism</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Mice</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>RNA Transport</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Signal Transduction</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Tumor Burden - genetics</subject><issn>1756-9966</issn><issn>0392-9078</issn><issn>1756-9966</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptksFq3DAQhk1oSdK0D9BLMRRKL041ki1Zl0IISVpYCITmLGR5vFawJVeyU_L2ldk03S1FhxGjb35JM3-WvQdyDlDzLxEYKXlBoCoIrUjBj7JTEBUvpOT81d7-JHsT4wMhHCTI4-yE8orVAOI0u99YZ0hSoPkU_OhnjOtmsB0GPVvvcuvyrY5zsCY32hkM-dwHv2z7FDG_urm-K1qc0LXo5nzSc_9LP73NXnd6iPjuOZ5l99dXPy6_FZvbm--XF5vCVBLmQjeIaBrDGs1bhrrVZSNTTjZVyVpDOQjsJANCsTTCmFp0opRac6pbEF3NzrKvO91paUZsTXpC0IOagh11eFJeW3V44myvtv5RlZxRynkS-PwsEPzPBeOsRhsNDoN26JeoQDAQdU0YTejHf9AHvwSXvpcoIevUWwF_qa0eUFnX-XSvWUXVRVnSqqS8Fok6_w-VVoujNd5hZ1P-oODTXkGPepj76IdlnVA8BGEHmuBjDNi9NAOIWk2jdqZRaeRqNY1am_Bhv4svFX9cwn4DR-m8ag</recordid><startdate>20151104</startdate><enddate>20151104</enddate><creator>Zhou, Jianping</creator><creator>Zhi, Xiaofei</creator><creator>Wang, Linjun</creator><creator>Wang, Weizhi</creator><creator>Li, Zheng</creator><creator>Tang, Jie</creator><creator>Wang, Jiwei</creator><creator>Zhang, Qun</creator><creator>Xu, Zekuan</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151104</creationdate><title>Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway</title><author>Zhou, Jianping ; Zhi, Xiaofei ; Wang, Linjun ; Wang, Weizhi ; Li, Zheng ; Tang, Jie ; Wang, Jiwei ; Zhang, Qun ; Xu, Zekuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c591t-abeeecbc3ba6d3eada4b9bee9b543dc2617ef93102e4c7cc87f749aa62ad17f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Care and treatment</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cholecystokinin</topic><topic>Complications and side effects</topic><topic>Cytoplasm - metabolism</topic><topic>Development and progression</topic><topic>Disease Models, Animal</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Mice</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>RNA Transport</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction</topic><topic>Stomach cancer</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Tumor Burden - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Jianping</creatorcontrib><creatorcontrib>Zhi, Xiaofei</creatorcontrib><creatorcontrib>Wang, Linjun</creatorcontrib><creatorcontrib>Wang, Weizhi</creatorcontrib><creatorcontrib>Li, Zheng</creatorcontrib><creatorcontrib>Tang, Jie</creatorcontrib><creatorcontrib>Wang, Jiwei</creatorcontrib><creatorcontrib>Zhang, Qun</creatorcontrib><creatorcontrib>Xu, Zekuan</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>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>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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 China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of experimental & clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Jianping</au><au>Zhi, Xiaofei</au><au>Wang, Linjun</au><au>Wang, Weizhi</au><au>Li, Zheng</au><au>Tang, Jie</au><au>Wang, Jiwei</au><au>Zhang, Qun</au><au>Xu, Zekuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway</atitle><jtitle>Journal of experimental & clinical cancer research</jtitle><addtitle>J Exp Clin Cancer Res</addtitle><date>2015-11-04</date><risdate>2015</risdate><volume>34</volume><issue>135</issue><spage>135</spage><epage>135</epage><pages>135-135</pages><artnum>135</artnum><issn>1756-9966</issn><issn>0392-9078</issn><eissn>1756-9966</eissn><abstract>Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear.
RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay.
In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling.
We first found that Linc00152 could promote tumor growth through EGFR-mediated PI3K/AKT pathway which may serve as potential targets for therapy in the future.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26538117</pmid><doi>10.1186/s13046-015-0250-6</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| source | SpringerOpen; MEDLINE; Springer Nature - Complete Springer Journals; DOAJ Directory of Open Access Journals; PubMed Central; EZB Electronic Journals Library; PubMed Central Open Access |
| subjects | Animals Care and treatment Cell Line, Tumor Cell Proliferation - genetics Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cholecystokinin Complications and side effects Cytoplasm - metabolism Development and progression Disease Models, Animal Heterografts Humans Mice Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Receptor, Epidermal Growth Factor - metabolism RNA Transport RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Tumor Burden - genetics |
| title | Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway |
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