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lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma
Long noncoding RNAs (lncRNAs) have been shown to play critical roles in cancer. lncTCF7 (gene symbol: WSPAR) has been reported to maintain stemness in hepatocellular carcinoma (HCC) stem cells. However, little is known about the role of lncTCF7 in glioma. The aim of this study was to identify the ro...
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Published in: | Scientific reports 2017-12, Vol.7 (1), p.17456-11, Article 17456 |
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description | Long noncoding RNAs (lncRNAs) have been shown to play critical roles in cancer.
lncTCF7
(gene symbol: WSPAR) has been reported to maintain stemness in hepatocellular carcinoma (HCC) stem cells. However, little is known about the role of
lncTCF7
in glioma. The aim of this study was to identify the role of
lncTCF7
in the pathogenesis of glioma. We analysed the relationship of
lncTCF7
expression with clinicopathological characteristics in glioma patients. Our results showed that
lncTCF7
expression was increased in glioma tissues compared with that in normal brain tissues (P |
doi_str_mv | 10.1038/s41598-017-17340-y |
format | article |
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lncTCF7
(gene symbol: WSPAR) has been reported to maintain stemness in hepatocellular carcinoma (HCC) stem cells. However, little is known about the role of
lncTCF7
in glioma. The aim of this study was to identify the role of
lncTCF7
in the pathogenesis of glioma. We analysed the relationship of
lncTCF7
expression with clinicopathological characteristics in glioma patients. Our results showed that
lncTCF7
expression was increased in glioma tissues compared with that in normal brain tissues (P < 0.001). Moreover,
lncTCF7
was significantly associated with WHO grade (I–II vs. III–IV; P = 0.006) and tumour size (<3 cm vs. T ≥ 3 cm; P = 0.025). Meanwhile, patients with high
lncTCF7
expression levels exhibited markedly worse overall survival prognoses (P < 0.01). Loss of function assays revealed that knockdown of
lncTCF7
significantly inhibited glioma cell migration, proliferation and tumorigenicity
in vitro
and
in vivo
. Furthermore, we found that hypoxia induced
lncTCF7
expression in an autocrine manner through IL-6 in glioma. In conclusion,
lncTCF7
may play a vital role in glioma progression and serves as a potential prognostic biomarker in glioma patients, providing new targets for glioma therapy.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-17340-y</identifier><identifier>PMID: 29234033</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/109 ; 13/31 ; 13/89 ; 14/34 ; 38/44 ; 38/77 ; 38/90 ; 631/67/1922 ; 631/67/395 ; 631/67/71 ; 64/600 ; 82/51 ; Adult ; Animals ; Autocrine signalling ; Brain - metabolism ; Brain - pathology ; Brain Neoplasms - metabolism ; Brain Neoplasms - mortality ; Brain Neoplasms - pathology ; Brain tumors ; Cell adhesion & migration ; Cell Hypoxia - physiology ; Cell Line, Tumor ; Cell migration ; Cell Movement - physiology ; Cell Proliferation - physiology ; Disease Progression ; Female ; Follow-Up Studies ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Glioma ; Glioma - metabolism ; Glioma - mortality ; Glioma - pathology ; Glioma cells ; Hepatocellular carcinoma ; Humanities and Social Sciences ; Humans ; Hypoxia ; Interleukin 6 ; Interleukin-6 - metabolism ; Male ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; multidisciplinary ; Neoplasm Transplantation ; Prognosis ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Science ; Science (multidisciplinary) ; Stem cells ; Tumorigenicity</subject><ispartof>Scientific reports, 2017-12, Vol.7 (1), p.17456-11, Article 17456</ispartof><rights>The Author(s) 2017</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-741d6ea52af2a7cd0d1fe44a9f5f383726955e70b9605d33f5bc27d2344affc63</citedby><cites>FETCH-LOGICAL-c474t-741d6ea52af2a7cd0d1fe44a9f5f383726955e70b9605d33f5bc27d2344affc63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1983424942/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1983424942?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29234033$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Xiao</creatorcontrib><creatorcontrib>Guo, Xing</creatorcontrib><creatorcontrib>Xue, Hao</creatorcontrib><creatorcontrib>Qiu, Wei</creatorcontrib><creatorcontrib>Guo, Xiaofan</creatorcontrib><creatorcontrib>Zhang, Jinsen</creatorcontrib><creatorcontrib>Qian, Mingyu</creatorcontrib><creatorcontrib>Li, Tong</creatorcontrib><creatorcontrib>Liu, Qinglin</creatorcontrib><creatorcontrib>Shen, Jie</creatorcontrib><creatorcontrib>Deng, Lin</creatorcontrib><creatorcontrib>Li, Gang</creatorcontrib><title>lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Long noncoding RNAs (lncRNAs) have been shown to play critical roles in cancer.
lncTCF7
(gene symbol: WSPAR) has been reported to maintain stemness in hepatocellular carcinoma (HCC) stem cells. However, little is known about the role of
lncTCF7
in glioma. The aim of this study was to identify the role of
lncTCF7
in the pathogenesis of glioma. We analysed the relationship of
lncTCF7
expression with clinicopathological characteristics in glioma patients. Our results showed that
lncTCF7
expression was increased in glioma tissues compared with that in normal brain tissues (P < 0.001). Moreover,
lncTCF7
was significantly associated with WHO grade (I–II vs. III–IV; P = 0.006) and tumour size (<3 cm vs. T ≥ 3 cm; P = 0.025). Meanwhile, patients with high
lncTCF7
expression levels exhibited markedly worse overall survival prognoses (P < 0.01). Loss of function assays revealed that knockdown of
lncTCF7
significantly inhibited glioma cell migration, proliferation and tumorigenicity
in vitro
and
in vivo
. Furthermore, we found that hypoxia induced
lncTCF7
expression in an autocrine manner through IL-6 in glioma. In conclusion,
lncTCF7
may play a vital role in glioma progression and serves as a potential prognostic biomarker in glioma patients, providing new targets for glioma therapy.</description><subject>13/1</subject><subject>13/109</subject><subject>13/31</subject><subject>13/89</subject><subject>14/34</subject><subject>38/44</subject><subject>38/77</subject><subject>38/90</subject><subject>631/67/1922</subject><subject>631/67/395</subject><subject>631/67/71</subject><subject>64/600</subject><subject>82/51</subject><subject>Adult</subject><subject>Animals</subject><subject>Autocrine signalling</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - mortality</subject><subject>Brain Neoplasms - pathology</subject><subject>Brain tumors</subject><subject>Cell adhesion & migration</subject><subject>Cell Hypoxia - physiology</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - physiology</subject><subject>Cell Proliferation - physiology</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Glioma</subject><subject>Glioma - metabolism</subject><subject>Glioma - mortality</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Hepatocellular carcinoma</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Male</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>multidisciplinary</subject><subject>Neoplasm Transplantation</subject><subject>Prognosis</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Stem cells</subject><subject>Tumorigenicity</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNp1kU9rHCEYhyW0NCHNF8ghCL30kGn9O46XQlmathDoJTmL6-jEZEa36iTsrR-9biZdtoV6UXmf59WXHwDnGH3AiHYfM8Ncdg3CosGCMtRsj8AJQYw3hBLy6uB8DM5yvkd1cSIZlm_AMZGkKpSegF9jMDerKwF9hhoGO-jiHy3cpDiEmIs30GlTYrqEOvTwIUTz0MenAKODezPc-bUvGU5-SFWP4XLnj97Z5fqslnmKyQ82eOPLtkpwGH2c9Fvw2ukx27OX_RTcXn25WX1rrn98_b76fN0YJlhpBMN9azUn2hEtTI967CxjWjruaEcFaSXnVqC1bBHvKXV8bYjo65hMO2daego-LX0383qyvbGhJD2qTfKTTlsVtVd_V4K_U0N8VFwQgduuNnj_0iDFn7PNRU0-GzuOOtg4Z4WlaBnrKNuh7_5B7-OcQh2vUpUgTDJSKbJQJsWck3X7z2CkdhmrJWNVM1bPGattlS4Ox9grfxKtAF2AXEthsOng7f-3_Q3uv7Sx</recordid><startdate>20171212</startdate><enddate>20171212</enddate><creator>Gao, Xiao</creator><creator>Guo, Xing</creator><creator>Xue, Hao</creator><creator>Qiu, Wei</creator><creator>Guo, Xiaofan</creator><creator>Zhang, Jinsen</creator><creator>Qian, Mingyu</creator><creator>Li, Tong</creator><creator>Liu, Qinglin</creator><creator>Shen, Jie</creator><creator>Deng, Lin</creator><creator>Li, Gang</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171212</creationdate><title>lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma</title><author>Gao, Xiao ; Guo, Xing ; Xue, Hao ; Qiu, Wei ; Guo, Xiaofan ; Zhang, Jinsen ; Qian, Mingyu ; Li, Tong ; Liu, Qinglin ; Shen, Jie ; Deng, Lin ; Li, Gang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-741d6ea52af2a7cd0d1fe44a9f5f383726955e70b9605d33f5bc27d2344affc63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13/1</topic><topic>13/109</topic><topic>13/31</topic><topic>13/89</topic><topic>14/34</topic><topic>38/44</topic><topic>38/77</topic><topic>38/90</topic><topic>631/67/1922</topic><topic>631/67/395</topic><topic>631/67/71</topic><topic>64/600</topic><topic>82/51</topic><topic>Adult</topic><topic>Animals</topic><topic>Autocrine signalling</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Neoplasms - metabolism</topic><topic>Brain Neoplasms - mortality</topic><topic>Brain Neoplasms - pathology</topic><topic>Brain tumors</topic><topic>Cell adhesion & migration</topic><topic>Cell Hypoxia - physiology</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - physiology</topic><topic>Cell Proliferation - physiology</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Glioma</topic><topic>Glioma - metabolism</topic><topic>Glioma - mortality</topic><topic>Glioma - pathology</topic><topic>Glioma cells</topic><topic>Hepatocellular carcinoma</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>Male</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>multidisciplinary</topic><topic>Neoplasm Transplantation</topic><topic>Prognosis</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Stem cells</topic><topic>Tumorigenicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Xiao</creatorcontrib><creatorcontrib>Guo, Xing</creatorcontrib><creatorcontrib>Xue, Hao</creatorcontrib><creatorcontrib>Qiu, Wei</creatorcontrib><creatorcontrib>Guo, Xiaofan</creatorcontrib><creatorcontrib>Zhang, Jinsen</creatorcontrib><creatorcontrib>Qian, Mingyu</creatorcontrib><creatorcontrib>Li, Tong</creatorcontrib><creatorcontrib>Liu, Qinglin</creatorcontrib><creatorcontrib>Shen, Jie</creatorcontrib><creatorcontrib>Deng, Lin</creatorcontrib><creatorcontrib>Li, Gang</creatorcontrib><collection>SpringerOpen</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>ProQuest 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)</collection><collection>ProQuest One Sustainability</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Publicly Available Content (ProQuest)</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>MEDLINE - Academic</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>Gao, Xiao</au><au>Guo, Xing</au><au>Xue, Hao</au><au>Qiu, Wei</au><au>Guo, Xiaofan</au><au>Zhang, Jinsen</au><au>Qian, Mingyu</au><au>Li, Tong</au><au>Liu, Qinglin</au><au>Shen, Jie</au><au>Deng, Lin</au><au>Li, Gang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-12-12</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>17456</spage><epage>11</epage><pages>17456-11</pages><artnum>17456</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Long noncoding RNAs (lncRNAs) have been shown to play critical roles in cancer.
lncTCF7
(gene symbol: WSPAR) has been reported to maintain stemness in hepatocellular carcinoma (HCC) stem cells. However, little is known about the role of
lncTCF7
in glioma. The aim of this study was to identify the role of
lncTCF7
in the pathogenesis of glioma. We analysed the relationship of
lncTCF7
expression with clinicopathological characteristics in glioma patients. Our results showed that
lncTCF7
expression was increased in glioma tissues compared with that in normal brain tissues (P < 0.001). Moreover,
lncTCF7
was significantly associated with WHO grade (I–II vs. III–IV; P = 0.006) and tumour size (<3 cm vs. T ≥ 3 cm; P = 0.025). Meanwhile, patients with high
lncTCF7
expression levels exhibited markedly worse overall survival prognoses (P < 0.01). Loss of function assays revealed that knockdown of
lncTCF7
significantly inhibited glioma cell migration, proliferation and tumorigenicity
in vitro
and
in vivo
. Furthermore, we found that hypoxia induced
lncTCF7
expression in an autocrine manner through IL-6 in glioma. In conclusion,
lncTCF7
may play a vital role in glioma progression and serves as a potential prognostic biomarker in glioma patients, providing new targets for glioma therapy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29234033</pmid><doi>10.1038/s41598-017-17340-y</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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source | Open Access: PubMed Central; Full-Text Journals in Chemistry (Open access); Publicly Available Content (ProQuest); Springer Nature - nature.com Journals - Fully Open Access |
subjects | 13/1 13/109 13/31 13/89 14/34 38/44 38/77 38/90 631/67/1922 631/67/395 631/67/71 64/600 82/51 Adult Animals Autocrine signalling Brain - metabolism Brain - pathology Brain Neoplasms - metabolism Brain Neoplasms - mortality Brain Neoplasms - pathology Brain tumors Cell adhesion & migration Cell Hypoxia - physiology Cell Line, Tumor Cell migration Cell Movement - physiology Cell Proliferation - physiology Disease Progression Female Follow-Up Studies Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Glioma Glioma - metabolism Glioma - mortality Glioma - pathology Glioma cells Hepatocellular carcinoma Humanities and Social Sciences Humans Hypoxia Interleukin 6 Interleukin-6 - metabolism Male Mice, Inbred BALB C Mice, Nude Middle Aged multidisciplinary Neoplasm Transplantation Prognosis RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Science Science (multidisciplinary) Stem cells Tumorigenicity |
title | lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma |
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