Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration
Long noncoding RNAs (lncRNAs), a novel class of transcripts that have critical roles in carcinogenesis and progression, have emerged as important gene expression modulators. Recent evidence indicates that lncRNA taurine‐upregulated gene 1 (TUG1) functions as an oncogene in numerous types of human ca...
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description | Long noncoding RNAs (lncRNAs), a novel class of transcripts that have critical roles in carcinogenesis and progression, have emerged as important gene expression modulators. Recent evidence indicates that lncRNA taurine‐upregulated gene 1 (TUG1) functions as an oncogene in numerous types of human cancers. However, its function in the development of cervical cancer remains unknown. The aim of this research was to investigate the clinical significance and biological functions of TUG1 in cervical cancer. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real‐time polymerase chain reaction (qRT‐PCR). Elevated TUG1 expression was correlated with larger tumor size, advanced international federation of gynecology and obstetrics (FIGO) stage, poor differentiation, and lymph node metastasis. Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl‐2 and caspase‐3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial–mesenchymal transition (EMT). Taken together, our findings indicate that TUG1 acts as an oncogene in cervical cancer and may represent a novel therapeutic target.
LncRNA TUG1 expression was significantly upregulated in cervical cancer and correlated with tumor size, international federation of gynecology and obstetrics (FIGO) stage, cell differentiation, and lymph node metastasis. Knockdown of TUG1 expression in cervical cancer cells inhibited cell proliferation and promoted cell apoptosis. Knockdown of TUG1 expression inhibited migration and invasion of cervical cancer cells via the mechanism of epithelial–mesenchymal transition (EMT). |
doi_str_mv | 10.1002/cam4.994 |
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LncRNA TUG1 expression was significantly upregulated in cervical cancer and correlated with tumor size, international federation of gynecology and obstetrics (FIGO) stage, cell differentiation, and lymph node metastasis. Knockdown of TUG1 expression in cervical cancer cells inhibited cell proliferation and promoted cell apoptosis. Knockdown of TUG1 expression inhibited migration and invasion of cervical cancer cells via the mechanism of epithelial–mesenchymal transition (EMT).</description><identifier>ISSN: 2045-7634</identifier><identifier>EISSN: 2045-7634</identifier><identifier>DOI: 10.1002/cam4.994</identifier><identifier>PMID: 28088836</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Apoptosis ; Bcl‐2 ; Cancer Biology ; Carcinogenesis ; Caspase ; Caspase 3 - genetics ; Cell activation ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Cervical cancer ; DNA methylation ; Epithelial-Mesenchymal Transition ; Ethics ; Experiments ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genomes ; Gynecology ; HeLa Cells ; Human papillomavirus ; Humans ; LncRNA ; Lymph nodes ; Lymphatic Metastasis ; Lymphatic system ; Mesenchyme ; Metastases ; Metastasis ; Neoplasm Staging ; Obstetrics ; Original Research ; Polymerase chain reaction ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Ribonucleic acid ; RNA ; RNA polymerase ; RNA, Long Noncoding - genetics ; Taurine ; Therapeutic applications ; TUG1 ; Tumor cell lines ; Up-Regulation ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - pathology ; Womens health</subject><ispartof>Cancer medicine (Malden, MA), 2017-02, Vol.6 (2), p.471-482</ispartof><rights>2016 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2016 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.</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-c5044-6df32f9420a350458f0d456cd1f89978254fb1805d6ba9aecb3317e5e587932c3</citedby><cites>FETCH-LOGICAL-c5044-6df32f9420a350458f0d456cd1f89978254fb1805d6ba9aecb3317e5e587932c3</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/PMC5313648/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5313648/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28088836$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Yingying</creatorcontrib><creatorcontrib>Sun, Xiangwei</creatorcontrib><creatorcontrib>Mao, Chenchen</creatorcontrib><creatorcontrib>Guo, Gangqiang</creatorcontrib><creatorcontrib>Ye, Sisi</creatorcontrib><creatorcontrib>Xu, Jianfeng</creatorcontrib><creatorcontrib>Zou, Ruanmin</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Wang, Ledan</creatorcontrib><creatorcontrib>Duan, Ping</creatorcontrib><creatorcontrib>Xue, Xiangyang</creatorcontrib><title>Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration</title><title>Cancer medicine (Malden, MA)</title><addtitle>Cancer Med</addtitle><description>Long noncoding RNAs (lncRNAs), a novel class of transcripts that have critical roles in carcinogenesis and progression, have emerged as important gene expression modulators. Recent evidence indicates that lncRNA taurine‐upregulated gene 1 (TUG1) functions as an oncogene in numerous types of human cancers. However, its function in the development of cervical cancer remains unknown. The aim of this research was to investigate the clinical significance and biological functions of TUG1 in cervical cancer. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real‐time polymerase chain reaction (qRT‐PCR). Elevated TUG1 expression was correlated with larger tumor size, advanced international federation of gynecology and obstetrics (FIGO) stage, poor differentiation, and lymph node metastasis. Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl‐2 and caspase‐3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial–mesenchymal transition (EMT). Taken together, our findings indicate that TUG1 acts as an oncogene in cervical cancer and may represent a novel therapeutic target.
LncRNA TUG1 expression was significantly upregulated in cervical cancer and correlated with tumor size, international federation of gynecology and obstetrics (FIGO) stage, cell differentiation, and lymph node metastasis. Knockdown of TUG1 expression in cervical cancer cells inhibited cell proliferation and promoted cell apoptosis. Knockdown of TUG1 expression inhibited migration and invasion of cervical cancer cells via the mechanism of epithelial–mesenchymal transition (EMT).</description><subject>Apoptosis</subject><subject>Bcl‐2</subject><subject>Cancer Biology</subject><subject>Carcinogenesis</subject><subject>Caspase</subject><subject>Caspase 3 - genetics</subject><subject>Cell activation</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cervical cancer</subject><subject>DNA methylation</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Ethics</subject><subject>Experiments</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genomes</subject><subject>Gynecology</subject><subject>HeLa Cells</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>LncRNA</subject><subject>Lymph nodes</subject><subject>Lymphatic Metastasis</subject><subject>Lymphatic system</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Neoplasm Staging</subject><subject>Obstetrics</subject><subject>Original Research</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA polymerase</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Taurine</subject><subject>Therapeutic applications</subject><subject>TUG1</subject><subject>Tumor cell lines</subject><subject>Up-Regulation</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Uterine Cervical Neoplasms - pathology</subject><subject>Womens health</subject><issn>2045-7634</issn><issn>2045-7634</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc1KAzEUhYMoWlTwCWTAjZvR_M4kG6EUrUJVkHYd0kxSUzJJzbSKb2_KqNSF2eTc3MN3LzkAnCF4hSDE11q19EoIugcGGFJW1hWh-zv6CJx23RLmU0Nc1egQHGEOOeekGgA1WyWz2Hi1djEU0RY-hkURYtCxcVm9PA2L6WyMilWKbVybrtAmvTutfKFVyDrX3m-73lmTeowKTdG6RV-dgAOrfGdOv-9jMLu7nY7uy8nz-GE0nJSaQUrLqrEEW0ExVCQ_MG5hQ1mlG2S5EDXHjNo54pA11VwJZfScEFQbZhivBcGaHIObnrvazFvTaBPWSXm5Sq5V6VNG5eTfTnCvchHfJSOIVJRnwMU3IMW3jenWchk3KeSdJcYCCsgphdl12bt0il2XjP2dgKDc5iG3ecicR7ae7270a_z5_Wwoe8OH8-bzX5AcDR_pFvgF8FiUiA</recordid><startdate>201702</startdate><enddate>201702</enddate><creator>Hu, Yingying</creator><creator>Sun, Xiangwei</creator><creator>Mao, Chenchen</creator><creator>Guo, Gangqiang</creator><creator>Ye, Sisi</creator><creator>Xu, Jianfeng</creator><creator>Zou, Ruanmin</creator><creator>Chen, Jun</creator><creator>Wang, Ledan</creator><creator>Duan, Ping</creator><creator>Xue, Xiangyang</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</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>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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PKEHL</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>201702</creationdate><title>Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration</title><author>Hu, Yingying ; Sun, Xiangwei ; Mao, Chenchen ; Guo, Gangqiang ; Ye, Sisi ; Xu, Jianfeng ; Zou, Ruanmin ; Chen, Jun ; Wang, Ledan ; Duan, Ping ; Xue, Xiangyang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5044-6df32f9420a350458f0d456cd1f89978254fb1805d6ba9aecb3317e5e587932c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Apoptosis</topic><topic>Bcl‐2</topic><topic>Cancer Biology</topic><topic>Carcinogenesis</topic><topic>Caspase</topic><topic>Caspase 3 - genetics</topic><topic>Cell activation</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cervical cancer</topic><topic>DNA methylation</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Ethics</topic><topic>Experiments</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genomes</topic><topic>Gynecology</topic><topic>HeLa Cells</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>LncRNA</topic><topic>Lymph nodes</topic><topic>Lymphatic Metastasis</topic><topic>Lymphatic system</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Neoplasm Staging</topic><topic>Obstetrics</topic><topic>Original Research</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA polymerase</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Taurine</topic><topic>Therapeutic applications</topic><topic>TUG1</topic><topic>Tumor cell lines</topic><topic>Up-Regulation</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - pathology</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Yingying</creatorcontrib><creatorcontrib>Sun, Xiangwei</creatorcontrib><creatorcontrib>Mao, Chenchen</creatorcontrib><creatorcontrib>Guo, Gangqiang</creatorcontrib><creatorcontrib>Ye, Sisi</creatorcontrib><creatorcontrib>Xu, Jianfeng</creatorcontrib><creatorcontrib>Zou, Ruanmin</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Wang, Ledan</creatorcontrib><creatorcontrib>Duan, Ping</creatorcontrib><creatorcontrib>Xue, Xiangyang</creatorcontrib><collection>Wiley Online Library Open Access</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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 Central Student</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>Biological Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer medicine (Malden, MA)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Yingying</au><au>Sun, Xiangwei</au><au>Mao, Chenchen</au><au>Guo, Gangqiang</au><au>Ye, Sisi</au><au>Xu, Jianfeng</au><au>Zou, Ruanmin</au><au>Chen, Jun</au><au>Wang, Ledan</au><au>Duan, Ping</au><au>Xue, Xiangyang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration</atitle><jtitle>Cancer medicine (Malden, MA)</jtitle><addtitle>Cancer Med</addtitle><date>2017-02</date><risdate>2017</risdate><volume>6</volume><issue>2</issue><spage>471</spage><epage>482</epage><pages>471-482</pages><issn>2045-7634</issn><eissn>2045-7634</eissn><abstract>Long noncoding RNAs (lncRNAs), a novel class of transcripts that have critical roles in carcinogenesis and progression, have emerged as important gene expression modulators. Recent evidence indicates that lncRNA taurine‐upregulated gene 1 (TUG1) functions as an oncogene in numerous types of human cancers. However, its function in the development of cervical cancer remains unknown. The aim of this research was to investigate the clinical significance and biological functions of TUG1 in cervical cancer. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real‐time polymerase chain reaction (qRT‐PCR). Elevated TUG1 expression was correlated with larger tumor size, advanced international federation of gynecology and obstetrics (FIGO) stage, poor differentiation, and lymph node metastasis. Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl‐2 and caspase‐3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial–mesenchymal transition (EMT). Taken together, our findings indicate that TUG1 acts as an oncogene in cervical cancer and may represent a novel therapeutic target.
LncRNA TUG1 expression was significantly upregulated in cervical cancer and correlated with tumor size, international federation of gynecology and obstetrics (FIGO) stage, cell differentiation, and lymph node metastasis. Knockdown of TUG1 expression in cervical cancer cells inhibited cell proliferation and promoted cell apoptosis. Knockdown of TUG1 expression inhibited migration and invasion of cervical cancer cells via the mechanism of epithelial–mesenchymal transition (EMT).</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>28088836</pmid><doi>10.1002/cam4.994</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis Bcl‐2 Cancer Biology Carcinogenesis Caspase Caspase 3 - genetics Cell activation Cell growth Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cervical cancer DNA methylation Epithelial-Mesenchymal Transition Ethics Experiments Female Gene expression Gene Expression Regulation, Neoplastic Genomes Gynecology HeLa Cells Human papillomavirus Humans LncRNA Lymph nodes Lymphatic Metastasis Lymphatic system Mesenchyme Metastases Metastasis Neoplasm Staging Obstetrics Original Research Polymerase chain reaction Proteins Proto-Oncogene Proteins c-bcl-2 - genetics Ribonucleic acid RNA RNA polymerase RNA, Long Noncoding - genetics Taurine Therapeutic applications TUG1 Tumor cell lines Up-Regulation Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - pathology Womens health |
title | Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration |
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