LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression
Gastric cancer (GC) is a highly prevalent type of metastatic tumor. The mechanisms underlying GC metastasis are poorly understood. Some long noncoding RNAs (lncRNAs) reportedly play key roles in regulating metastasis of GC. However, the biological roles of five natural antisense lncRNAs (AC093818.1,...
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| Veröffentlicht in: | Cell death & disease 2020-01, Vol.11 (1), p.64-64, Article 64 |
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| description | Gastric cancer (GC) is a highly prevalent type of metastatic tumor. The mechanisms underlying GC metastasis are poorly understood. Some long noncoding RNAs (lncRNAs) reportedly play key roles in regulating metastasis of GC. However, the biological roles of five natural antisense lncRNAs (AC093818.1, CTD-2541M15.1, BC047644, RP11-597M12.1, and RP11-40A13.1) in GC metastasis remain unclear. In this study, the expression of these lncRNAs was measured by quantitative reverse transcription-polymerase chain reaction. Migration and invasion were evaluated by wound-healing and the Transwell assay, respectively. Stable cells were injected into the tail veins of nude mice. Sections of collected lung and liver tissues were stained using hematoxylin and eosin. Protein expression was analyzed by western blot. RNA immunoprecipitation (RIP) assay was used to verify whether the STAT3 and SP1 transcription factors bound to AC093818.1 in GC cells. Expression levels of the five lncRNAs, especially AC093818.1, were significantly upregulated in metastatic GC tissues relative to those in nonmetastatic GC tissues. AC093818.1 expression was correlated with invasion, lymphatic metastasis, distal metastasis, and tumor-node-metastasis stage. AC093818.1 expression was highly sensitive and specific in the diagnosis of metastatic or nonmetastatic GC. AC093818.1 overexpression promoted GC migration and invasion in vitro and in vivo. AC093818.1 overexpression increased PDK1, p-AKT1, and p-mTOR expression levels. AC093818.1 silencing decreased these expressions. AC093818.1 bound to transcription factors STAT3 and SP1, and SP1 or STAT3 silencing could alleviated the effect of AC093818.1 overexpression. The data demonstrate that lncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression. LncRNA AC093818.1 may be a potential therapeutic target for metastatic GC. |
| doi_str_mv | 10.1038/s41419-020-2245-2 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6985138</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2347507331</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-e28c2d9c1adf815620e6a0bee8257dbd88c4abcecea682d13f2f64165c03442d3</originalsourceid><addsrcrecordid>eNp1kcFu1DAQhi0EotXSB-CCLHHhkuKxHa9zQVot0CJWgBCcLceZBFeJHewsYt8er7aUgoQvY3m--cczPyFPgV0CE_plliChqRhnFeeyrvgDcs6ZhEpq3Ty8dz8jFznfsHKEYLxWj8mZgEZrrsU5cbvgPn_Y0M2WNUKDvgRqncMRk10w08HmJXlHnQ0OE51wKQ82-0zbA8XZDxhw8c6O44HOKU5x8WGgn16_B4o_54Q5-xiekEe9HTNe3MYV-fr2zZftdbX7ePVuu9lVTq7ZUiHXjneNA9v1GmrFGSrLWkTN63XXdlo7aVuHDq3SvAPR815JULVjQkreiRV5ddKd9-2EncOwJDuaOfnJpoOJ1pu_M8F_M0P8YVSjaxC6CLy4FUjx-x7zYiafyzJGGzDus-FCrmu2FgIK-vwf9CbuUyjjHSklmWxUUyg4US7FnBP2d58BZo4umpOLprhoji6W4hV5dn-Ku4rfnhWAn4BcUmHA9Kf1_1V_ARS7p7A</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2346404969</pqid></control><display><type>article</type><title>LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Springer Nature OA Free Journals</source><source>Nature Free</source><source>PubMed Central</source><creator>Ba, Ming-chen ; Ba, Zheng ; Long, Hui ; Cui, Shu-zhong ; Gong, Yuan-feng ; Yan, Zhao-fei ; Lin, Kun-peng ; Wu, Yin-bing ; Tu, Yi-nuo</creator><creatorcontrib>Ba, Ming-chen ; Ba, Zheng ; Long, Hui ; Cui, Shu-zhong ; Gong, Yuan-feng ; Yan, Zhao-fei ; Lin, Kun-peng ; Wu, Yin-bing ; Tu, Yi-nuo</creatorcontrib><description>Gastric cancer (GC) is a highly prevalent type of metastatic tumor. The mechanisms underlying GC metastasis are poorly understood. Some long noncoding RNAs (lncRNAs) reportedly play key roles in regulating metastasis of GC. However, the biological roles of five natural antisense lncRNAs (AC093818.1, CTD-2541M15.1, BC047644, RP11-597M12.1, and RP11-40A13.1) in GC metastasis remain unclear. In this study, the expression of these lncRNAs was measured by quantitative reverse transcription-polymerase chain reaction. Migration and invasion were evaluated by wound-healing and the Transwell assay, respectively. Stable cells were injected into the tail veins of nude mice. Sections of collected lung and liver tissues were stained using hematoxylin and eosin. Protein expression was analyzed by western blot. RNA immunoprecipitation (RIP) assay was used to verify whether the STAT3 and SP1 transcription factors bound to AC093818.1 in GC cells. Expression levels of the five lncRNAs, especially AC093818.1, were significantly upregulated in metastatic GC tissues relative to those in nonmetastatic GC tissues. AC093818.1 expression was correlated with invasion, lymphatic metastasis, distal metastasis, and tumor-node-metastasis stage. AC093818.1 expression was highly sensitive and specific in the diagnosis of metastatic or nonmetastatic GC. AC093818.1 overexpression promoted GC migration and invasion in vitro and in vivo. AC093818.1 overexpression increased PDK1, p-AKT1, and p-mTOR expression levels. AC093818.1 silencing decreased these expressions. AC093818.1 bound to transcription factors STAT3 and SP1, and SP1 or STAT3 silencing could alleviated the effect of AC093818.1 overexpression. The data demonstrate that lncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression. LncRNA AC093818.1 may be a potential therapeutic target for metastatic GC.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2245-2</identifier><identifier>PMID: 31988283</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/95 ; 38/77 ; 38/89 ; 42/89 ; 631/67/1680 ; 692/53/2421 ; 82/80 ; AKT1 protein ; Animals ; Antibodies ; Antisense therapy ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Cell Line, Tumor ; Cell Movement - genetics ; Epigenesis, Genetic ; Female ; Gastric cancer ; Gene Silencing ; Humans ; Immunology ; Immunoprecipitation ; Life Sciences ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - secondary ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - secondary ; Lymphatic Metastasis - genetics ; Male ; Metastases ; Metastasis ; Mice ; Mice, Nude ; Middle Aged ; Neoplasm Staging ; Polymerase chain reaction ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase - genetics ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase - metabolism ; Reverse transcription ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; RNA, Small Interfering ; Sp1 protein ; Sp1 Transcription Factor - genetics ; Sp1 Transcription Factor - metabolism ; Stat3 protein ; STAT3 Transcription Factor - genetics ; STAT3 Transcription Factor - metabolism ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Therapeutic applications ; TOR protein ; TOR Serine-Threonine Kinases - genetics ; TOR Serine-Threonine Kinases - metabolism ; Transcription factors ; Up-Regulation ; Wound healing</subject><ispartof>Cell death & disease, 2020-01, Vol.11 (1), p.64-64, Article 64</ispartof><rights>The Author(s) 2020</rights><rights>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-c470t-e28c2d9c1adf815620e6a0bee8257dbd88c4abcecea682d13f2f64165c03442d3</citedby><cites>FETCH-LOGICAL-c470t-e28c2d9c1adf815620e6a0bee8257dbd88c4abcecea682d13f2f64165c03442d3</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/PMC6985138/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6985138/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,41119,42188,51575,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31988283$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ba, Ming-chen</creatorcontrib><creatorcontrib>Ba, Zheng</creatorcontrib><creatorcontrib>Long, Hui</creatorcontrib><creatorcontrib>Cui, Shu-zhong</creatorcontrib><creatorcontrib>Gong, Yuan-feng</creatorcontrib><creatorcontrib>Yan, Zhao-fei</creatorcontrib><creatorcontrib>Lin, Kun-peng</creatorcontrib><creatorcontrib>Wu, Yin-bing</creatorcontrib><creatorcontrib>Tu, Yi-nuo</creatorcontrib><title>LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Gastric cancer (GC) is a highly prevalent type of metastatic tumor. The mechanisms underlying GC metastasis are poorly understood. Some long noncoding RNAs (lncRNAs) reportedly play key roles in regulating metastasis of GC. However, the biological roles of five natural antisense lncRNAs (AC093818.1, CTD-2541M15.1, BC047644, RP11-597M12.1, and RP11-40A13.1) in GC metastasis remain unclear. In this study, the expression of these lncRNAs was measured by quantitative reverse transcription-polymerase chain reaction. Migration and invasion were evaluated by wound-healing and the Transwell assay, respectively. Stable cells were injected into the tail veins of nude mice. Sections of collected lung and liver tissues were stained using hematoxylin and eosin. Protein expression was analyzed by western blot. RNA immunoprecipitation (RIP) assay was used to verify whether the STAT3 and SP1 transcription factors bound to AC093818.1 in GC cells. Expression levels of the five lncRNAs, especially AC093818.1, were significantly upregulated in metastatic GC tissues relative to those in nonmetastatic GC tissues. AC093818.1 expression was correlated with invasion, lymphatic metastasis, distal metastasis, and tumor-node-metastasis stage. AC093818.1 expression was highly sensitive and specific in the diagnosis of metastatic or nonmetastatic GC. AC093818.1 overexpression promoted GC migration and invasion in vitro and in vivo. AC093818.1 overexpression increased PDK1, p-AKT1, and p-mTOR expression levels. AC093818.1 silencing decreased these expressions. AC093818.1 bound to transcription factors STAT3 and SP1, and SP1 or STAT3 silencing could alleviated the effect of AC093818.1 overexpression. The data demonstrate that lncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression. LncRNA AC093818.1 may be a potential therapeutic target for metastatic GC.</description><subject>13/95</subject><subject>38/77</subject><subject>38/89</subject><subject>42/89</subject><subject>631/67/1680</subject><subject>692/53/2421</subject><subject>82/80</subject><subject>AKT1 protein</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antisense therapy</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Epigenesis, Genetic</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>Immunology</subject><subject>Immunoprecipitation</subject><subject>Life Sciences</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - secondary</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - secondary</subject><subject>Lymphatic Metastasis - genetics</subject><subject>Male</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Neoplasm Staging</subject><subject>Polymerase chain reaction</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Pyruvate Dehydrogenase Acetyl-Transferring Kinase - genetics</subject><subject>Pyruvate Dehydrogenase Acetyl-Transferring Kinase - metabolism</subject><subject>Reverse transcription</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>RNA, Small Interfering</subject><subject>Sp1 protein</subject><subject>Sp1 Transcription Factor - genetics</subject><subject>Sp1 Transcription Factor - metabolism</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Therapeutic applications</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - genetics</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Transcription factors</subject><subject>Up-Regulation</subject><subject>Wound healing</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</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>eNp1kcFu1DAQhi0EotXSB-CCLHHhkuKxHa9zQVot0CJWgBCcLceZBFeJHewsYt8er7aUgoQvY3m--cczPyFPgV0CE_plliChqRhnFeeyrvgDcs6ZhEpq3Ty8dz8jFznfsHKEYLxWj8mZgEZrrsU5cbvgPn_Y0M2WNUKDvgRqncMRk10w08HmJXlHnQ0OE51wKQ82-0zbA8XZDxhw8c6O44HOKU5x8WGgn16_B4o_54Q5-xiekEe9HTNe3MYV-fr2zZftdbX7ePVuu9lVTq7ZUiHXjneNA9v1GmrFGSrLWkTN63XXdlo7aVuHDq3SvAPR815JULVjQkreiRV5ddKd9-2EncOwJDuaOfnJpoOJ1pu_M8F_M0P8YVSjaxC6CLy4FUjx-x7zYiafyzJGGzDus-FCrmu2FgIK-vwf9CbuUyjjHSklmWxUUyg4US7FnBP2d58BZo4umpOLprhoji6W4hV5dn-Ku4rfnhWAn4BcUmHA9Kf1_1V_ARS7p7A</recordid><startdate>20200127</startdate><enddate>20200127</enddate><creator>Ba, Ming-chen</creator><creator>Ba, Zheng</creator><creator>Long, Hui</creator><creator>Cui, Shu-zhong</creator><creator>Gong, Yuan-feng</creator><creator>Yan, Zhao-fei</creator><creator>Lin, Kun-peng</creator><creator>Wu, Yin-bing</creator><creator>Tu, Yi-nuo</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</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>88I</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>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200127</creationdate><title>LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression</title><author>Ba, Ming-chen ; Ba, Zheng ; Long, Hui ; Cui, Shu-zhong ; Gong, Yuan-feng ; Yan, Zhao-fei ; Lin, Kun-peng ; Wu, Yin-bing ; Tu, Yi-nuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-e28c2d9c1adf815620e6a0bee8257dbd88c4abcecea682d13f2f64165c03442d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/95</topic><topic>38/77</topic><topic>38/89</topic><topic>42/89</topic><topic>631/67/1680</topic><topic>692/53/2421</topic><topic>82/80</topic><topic>AKT1 protein</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antisense therapy</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Epigenesis, Genetic</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>Immunology</topic><topic>Immunoprecipitation</topic><topic>Life Sciences</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - secondary</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - secondary</topic><topic>Lymphatic Metastasis - genetics</topic><topic>Male</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Neoplasm Staging</topic><topic>Polymerase chain reaction</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Pyruvate Dehydrogenase Acetyl-Transferring Kinase - genetics</topic><topic>Pyruvate Dehydrogenase Acetyl-Transferring Kinase - metabolism</topic><topic>Reverse transcription</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>RNA, Small Interfering</topic><topic>Sp1 protein</topic><topic>Sp1 Transcription Factor - genetics</topic><topic>Sp1 Transcription Factor - metabolism</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Therapeutic applications</topic><topic>TOR protein</topic><topic>TOR Serine-Threonine Kinases - genetics</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Transcription factors</topic><topic>Up-Regulation</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ba, Ming-chen</creatorcontrib><creatorcontrib>Ba, Zheng</creatorcontrib><creatorcontrib>Long, Hui</creatorcontrib><creatorcontrib>Cui, Shu-zhong</creatorcontrib><creatorcontrib>Gong, Yuan-feng</creatorcontrib><creatorcontrib>Yan, Zhao-fei</creatorcontrib><creatorcontrib>Lin, Kun-peng</creatorcontrib><creatorcontrib>Wu, Yin-bing</creatorcontrib><creatorcontrib>Tu, Yi-nuo</creatorcontrib><collection>Springer Nature OA Free Journals</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>Biology 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 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>Science Database</collection><collection>Biological Science 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ba, Ming-chen</au><au>Ba, Zheng</au><au>Long, Hui</au><au>Cui, Shu-zhong</au><au>Gong, Yuan-feng</au><au>Yan, Zhao-fei</au><au>Lin, Kun-peng</au><au>Wu, Yin-bing</au><au>Tu, Yi-nuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-01-27</date><risdate>2020</risdate><volume>11</volume><issue>1</issue><spage>64</spage><epage>64</epage><pages>64-64</pages><artnum>64</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Gastric cancer (GC) is a highly prevalent type of metastatic tumor. The mechanisms underlying GC metastasis are poorly understood. Some long noncoding RNAs (lncRNAs) reportedly play key roles in regulating metastasis of GC. However, the biological roles of five natural antisense lncRNAs (AC093818.1, CTD-2541M15.1, BC047644, RP11-597M12.1, and RP11-40A13.1) in GC metastasis remain unclear. In this study, the expression of these lncRNAs was measured by quantitative reverse transcription-polymerase chain reaction. Migration and invasion were evaluated by wound-healing and the Transwell assay, respectively. Stable cells were injected into the tail veins of nude mice. Sections of collected lung and liver tissues were stained using hematoxylin and eosin. Protein expression was analyzed by western blot. RNA immunoprecipitation (RIP) assay was used to verify whether the STAT3 and SP1 transcription factors bound to AC093818.1 in GC cells. Expression levels of the five lncRNAs, especially AC093818.1, were significantly upregulated in metastatic GC tissues relative to those in nonmetastatic GC tissues. AC093818.1 expression was correlated with invasion, lymphatic metastasis, distal metastasis, and tumor-node-metastasis stage. AC093818.1 expression was highly sensitive and specific in the diagnosis of metastatic or nonmetastatic GC. AC093818.1 overexpression promoted GC migration and invasion in vitro and in vivo. AC093818.1 overexpression increased PDK1, p-AKT1, and p-mTOR expression levels. AC093818.1 silencing decreased these expressions. AC093818.1 bound to transcription factors STAT3 and SP1, and SP1 or STAT3 silencing could alleviated the effect of AC093818.1 overexpression. The data demonstrate that lncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression. LncRNA AC093818.1 may be a potential therapeutic target for metastatic GC.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31988283</pmid><doi>10.1038/s41419-020-2245-2</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6985138 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature OA Free Journals; Nature Free; PubMed Central |
| subjects | 13/95 38/77 38/89 42/89 631/67/1680 692/53/2421 82/80 AKT1 protein Animals Antibodies Antisense therapy Biochemistry Biomedical and Life Sciences Cell Biology Cell Culture Cell Line, Tumor Cell Movement - genetics Epigenesis, Genetic Female Gastric cancer Gene Silencing Humans Immunology Immunoprecipitation Life Sciences Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - secondary Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - secondary Lymphatic Metastasis - genetics Male Metastases Metastasis Mice Mice, Nude Middle Aged Neoplasm Staging Polymerase chain reaction Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Pyruvate Dehydrogenase Acetyl-Transferring Kinase - genetics Pyruvate Dehydrogenase Acetyl-Transferring Kinase - metabolism Reverse transcription Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA, Small Interfering Sp1 protein Sp1 Transcription Factor - genetics Sp1 Transcription Factor - metabolism Stat3 protein STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Therapeutic applications TOR protein TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism Transcription factors Up-Regulation Wound healing |
| title | LncRNA AC093818.1 accelerates gastric cancer metastasis by epigenetically promoting PDK1 expression |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-12T21%3A57%3A00IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=LncRNA%20AC093818.1%20accelerates%20gastric%20cancer%20metastasis%20by%20epigenetically%20promoting%20PDK1%20expression&rft.jtitle=Cell%20death%20&%20disease&rft.au=Ba,%20Ming-chen&rft.date=2020-01-27&rft.volume=11&rft.issue=1&rft.spage=64&rft.epage=64&rft.pages=64-64&rft.artnum=64&rft.issn=2041-4889&rft.eissn=2041-4889&rft_id=info:doi/10.1038/s41419-020-2245-2&rft_dat=%3Cproquest_pubme%3E2347507331%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2346404969&rft_id=info:pmid/31988283&rfr_iscdi=true |