CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis
Accumulating evidences indicate that 3ʹUTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that acvr1b gene 3ʹUTR ( acv 3UTR) was elevated in GC tissue, the expression of which w...
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| Veröffentlicht in: | Oncogene 2020-04, Vol.39 (15), p.3075-3088 |
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| creator | Liu, Kai Wang, Ben-Jun Han, WeiWei Chi, Chun-Hua Gu, Chao Wang, Yu Fu, Xiaohai Huang, Wei Liu, Zhiguo Song, Xilin |
| description | Accumulating evidences indicate that 3ʹUTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that
acvr1b
gene 3ʹUTR (
acv
3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of
acv
3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that
acv
3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in
acv
3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of
acv
3UTR. The positive correlation of
acv
3UTR and YAP1 expression, and the negative correlation of
acv
3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to
acv
3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of
acv
3UTR transcription in GC tumorigenesis, and indicates a correlation between 3ʹUTR
trans
-regulatory effect and GC development. |
| doi_str_mv | 10.1038/s41388-020-1213-8 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7142022</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A619849768</galeid><sourcerecordid>A619849768</sourcerecordid><originalsourceid>FETCH-LOGICAL-c565t-324fc44621987b8d20bd2c4c087aa9f4e2e4f09d38e4abff1b4e30f45aa5ac0a3</originalsourceid><addsrcrecordid>eNp9Uktr3DAYFKUl2Sb5Ab0UQ89KPr1s-VJYlqQNhKYsCaUnIcuSq2BbW8le2n9fLZvmAW3QQaBvZqQZDULvCJwSYPIsccKkxEABE0oYlq_QgvCqxELU_DVaQC0A15TRQ_Q2pTsAqGqgB-iQUShLWckF-ra6uByowNF2c68n2xb9aNZfloU2W3Z7sy42MQxhsqnodJqiN8U0DyH6zo42-VRsvS4Gv8aiBiw2Z9-XX0mhf_l0jN443Sd7cr8foduL85vVZ3x1_elytbzCRpRiwoxyZzgvKall1ciWQtNSww3ISuvacUstd1C3TFquG-dIwy0Dx4XWQhvQ7Ah93Otu5mawrbHjFHWvNtEPOv5WQXv1fDL6H6oLW1URToHSLPDhXiCGn7NNk7oLcxzzmxXNUVY5YCleRDFZlYxQAY-oTvdW-dGFfKUZfDJqWWaHvK5KmVGn_0Dl1drBmzBa5_P5MwLZE0wMKUXrHuwRULsiqH0RVC6C2hVB7Tjvn-bywPj78xlA94CUR2Nn46Oj_6v-Acy2uxc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2387631250</pqid></control><display><type>article</type><title>CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Liu, Kai ; Wang, Ben-Jun ; Han, WeiWei ; Chi, Chun-Hua ; Gu, Chao ; Wang, Yu ; Fu, Xiaohai ; Huang, Wei ; Liu, Zhiguo ; Song, Xilin</creator><creatorcontrib>Liu, Kai ; Wang, Ben-Jun ; Han, WeiWei ; Chi, Chun-Hua ; Gu, Chao ; Wang, Yu ; Fu, Xiaohai ; Huang, Wei ; Liu, Zhiguo ; Song, Xilin</creatorcontrib><description>Accumulating evidences indicate that 3ʹUTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that
acvr1b
gene 3ʹUTR (
acv
3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of
acv
3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that
acv
3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in
acv
3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of
acv
3UTR. The positive correlation of
acv
3UTR and YAP1 expression, and the negative correlation of
acv
3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to
acv
3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of
acv
3UTR transcription in GC tumorigenesis, and indicates a correlation between 3ʹUTR
trans
-regulatory effect and GC development.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-020-1213-8</identifier><identifier>PMID: 32066878</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>3' Untranslated Regions - genetics ; 631/45 ; 631/67/1504/1829 ; Activin Receptors, Type I - genetics ; ACVR1B gene ; Adaptor Proteins, Signal Transducing - genetics ; Animals ; Apoptosis ; Carcinogenesis - genetics ; Care and treatment ; Cell Biology ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cleavage And Polyadenylation Specificity Factor - metabolism ; Development and progression ; Disease Progression ; Female ; Gastric cancer ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Health aspects ; Human Genetics ; Humans ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Mice ; MicroRNA ; MicroRNAs - metabolism ; Middle Aged ; Oncology ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Stomach - pathology ; Stomach cancer ; Stomach Neoplasms - genetics ; Transcription ; Transcription Factors - genetics ; Transcription, Genetic ; Tumor suppressor genes ; Tumorigenesis ; Xenograft Model Antitumor Assays ; Yes-associated protein</subject><ispartof>Oncogene, 2020-04, Vol.39 (15), p.3075-3088</ispartof><rights>The Author(s) 2020</rights><rights>COPYRIGHT 2020 Nature Publishing Group</rights><rights>The Author(s) 2020. 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-c565t-324fc44621987b8d20bd2c4c087aa9f4e2e4f09d38e4abff1b4e30f45aa5ac0a3</citedby><cites>FETCH-LOGICAL-c565t-324fc44621987b8d20bd2c4c087aa9f4e2e4f09d38e4abff1b4e30f45aa5ac0a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32066878$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Kai</creatorcontrib><creatorcontrib>Wang, Ben-Jun</creatorcontrib><creatorcontrib>Han, WeiWei</creatorcontrib><creatorcontrib>Chi, Chun-Hua</creatorcontrib><creatorcontrib>Gu, Chao</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Fu, Xiaohai</creatorcontrib><creatorcontrib>Huang, Wei</creatorcontrib><creatorcontrib>Liu, Zhiguo</creatorcontrib><creatorcontrib>Song, Xilin</creatorcontrib><title>CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Accumulating evidences indicate that 3ʹUTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that
acvr1b
gene 3ʹUTR (
acv
3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of
acv
3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that
acv
3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in
acv
3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of
acv
3UTR. The positive correlation of
acv
3UTR and YAP1 expression, and the negative correlation of
acv
3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to
acv
3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of
acv
3UTR transcription in GC tumorigenesis, and indicates a correlation between 3ʹUTR
trans
-regulatory effect and GC development.</description><subject>3' Untranslated Regions - genetics</subject><subject>631/45</subject><subject>631/67/1504/1829</subject><subject>Activin Receptors, Type I - genetics</subject><subject>ACVR1B gene</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Carcinogenesis - genetics</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cleavage And Polyadenylation Specificity Factor - metabolism</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>MicroRNA</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Oncology</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Stomach - pathology</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Transcription</subject><subject>Transcription Factors - genetics</subject><subject>Transcription, Genetic</subject><subject>Tumor suppressor genes</subject><subject>Tumorigenesis</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Yes-associated protein</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9Uktr3DAYFKUl2Sb5Ab0UQ89KPr1s-VJYlqQNhKYsCaUnIcuSq2BbW8le2n9fLZvmAW3QQaBvZqQZDULvCJwSYPIsccKkxEABE0oYlq_QgvCqxELU_DVaQC0A15TRQ_Q2pTsAqGqgB-iQUShLWckF-ra6uByowNF2c68n2xb9aNZfloU2W3Z7sy42MQxhsqnodJqiN8U0DyH6zo42-VRsvS4Gv8aiBiw2Z9-XX0mhf_l0jN443Sd7cr8foduL85vVZ3x1_elytbzCRpRiwoxyZzgvKall1ciWQtNSww3ISuvacUstd1C3TFquG-dIwy0Dx4XWQhvQ7Ah93Otu5mawrbHjFHWvNtEPOv5WQXv1fDL6H6oLW1URToHSLPDhXiCGn7NNk7oLcxzzmxXNUVY5YCleRDFZlYxQAY-oTvdW-dGFfKUZfDJqWWaHvK5KmVGn_0Dl1drBmzBa5_P5MwLZE0wMKUXrHuwRULsiqH0RVC6C2hVB7Tjvn-bywPj78xlA94CUR2Nn46Oj_6v-Acy2uxc</recordid><startdate>20200409</startdate><enddate>20200409</enddate><creator>Liu, Kai</creator><creator>Wang, Ben-Jun</creator><creator>Han, WeiWei</creator><creator>Chi, Chun-Hua</creator><creator>Gu, Chao</creator><creator>Wang, Yu</creator><creator>Fu, Xiaohai</creator><creator>Huang, Wei</creator><creator>Liu, Zhiguo</creator><creator>Song, Xilin</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>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>8G5</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20200409</creationdate><title>CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis</title><author>Liu, Kai ; Wang, Ben-Jun ; Han, WeiWei ; Chi, Chun-Hua ; Gu, Chao ; Wang, Yu ; Fu, Xiaohai ; Huang, Wei ; Liu, Zhiguo ; Song, Xilin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-324fc44621987b8d20bd2c4c087aa9f4e2e4f09d38e4abff1b4e30f45aa5ac0a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>3' Untranslated Regions - genetics</topic><topic>631/45</topic><topic>631/67/1504/1829</topic><topic>Activin Receptors, Type I - genetics</topic><topic>ACVR1B gene</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Carcinogenesis - genetics</topic><topic>Care and treatment</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cleavage And Polyadenylation Specificity Factor - metabolism</topic><topic>Development and progression</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>MicroRNA</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Oncology</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Stomach - pathology</topic><topic>Stomach cancer</topic><topic>Stomach Neoplasms - genetics</topic><topic>Transcription</topic><topic>Transcription Factors - genetics</topic><topic>Transcription, Genetic</topic><topic>Tumor suppressor genes</topic><topic>Tumorigenesis</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Yes-associated protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Kai</creatorcontrib><creatorcontrib>Wang, Ben-Jun</creatorcontrib><creatorcontrib>Han, WeiWei</creatorcontrib><creatorcontrib>Chi, Chun-Hua</creatorcontrib><creatorcontrib>Gu, Chao</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Fu, Xiaohai</creatorcontrib><creatorcontrib>Huang, Wei</creatorcontrib><creatorcontrib>Liu, Zhiguo</creatorcontrib><creatorcontrib>Song, Xilin</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>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>Research Library (Alumni Edition)</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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Kai</au><au>Wang, Ben-Jun</au><au>Han, WeiWei</au><au>Chi, Chun-Hua</au><au>Gu, Chao</au><au>Wang, Yu</au><au>Fu, Xiaohai</au><au>Huang, Wei</au><au>Liu, Zhiguo</au><au>Song, Xilin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2020-04-09</date><risdate>2020</risdate><volume>39</volume><issue>15</issue><spage>3075</spage><epage>3088</epage><pages>3075-3088</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Accumulating evidences indicate that 3ʹUTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that
acvr1b
gene 3ʹUTR (
acv
3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of
acv
3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that
acv
3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in
acv
3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of
acv
3UTR. The positive correlation of
acv
3UTR and YAP1 expression, and the negative correlation of
acv
3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to
acv
3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of
acv
3UTR transcription in GC tumorigenesis, and indicates a correlation between 3ʹUTR
trans
-regulatory effect and GC development.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32066878</pmid><doi>10.1038/s41388-020-1213-8</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Oncogene, 2020-04, Vol.39 (15), p.3075-3088 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7142022 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | 3' Untranslated Regions - genetics 631/45 631/67/1504/1829 Activin Receptors, Type I - genetics ACVR1B gene Adaptor Proteins, Signal Transducing - genetics Animals Apoptosis Carcinogenesis - genetics Care and treatment Cell Biology Cell Line, Tumor Cell Proliferation - genetics Cleavage And Polyadenylation Specificity Factor - metabolism Development and progression Disease Progression Female Gastric cancer Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Health aspects Human Genetics Humans Internal Medicine Male Medicine Medicine & Public Health Mice MicroRNA MicroRNAs - metabolism Middle Aged Oncology Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Stomach - pathology Stomach cancer Stomach Neoplasms - genetics Transcription Transcription Factors - genetics Transcription, Genetic Tumor suppressor genes Tumorigenesis Xenograft Model Antitumor Assays Yes-associated protein |
| title | CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis |
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