F. nucleatum targets lncRNA ENO1-IT1 to promote glycolysis and oncogenesis in colorectal cancer
ObjectiveMicrobiota disorder promotes chronic inflammation and carcinogenesis. High glycolysis is associated with poor prognosis in patients with colorectal cancer (CRC). However, the potential correlation between the gut microbiota and glucose metabolism is unknown in CRC.Design 18F-FDG (18F-fluoro...
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| creator | Hong, Jie Guo, Fangfang Lu, Shi-Yuan Shen, Chaoqin Ma, Dan Zhang, Xinyu Xie, Yile Yan, Tingting Yu, TaChung Sun, Tiantian Qian, Yun Zhong, Ming Chen, Jinxian Peng, Yanshen Wang, Cheng Zhou, Xiang Liu, Jianjun Liu, Qiang Ma, Xiong Chen, Ying-Xuan Chen, Haoyan Fang, Jing-Yuan |
| description | ObjectiveMicrobiota disorder promotes chronic inflammation and carcinogenesis. High glycolysis is associated with poor prognosis in patients with colorectal cancer (CRC). However, the potential correlation between the gut microbiota and glucose metabolism is unknown in CRC.Design 18F-FDG (18F-fluorodeoxyglucose) PET (positron emission tomography)/CT image scanning data and microbiota PCR analysis were performed to measure the correlation between metabolic alterations and microbiota disorder in 33 patients with CRC. Multiple colorectal cancer models, metabolic analysis and Seahorse assay were established to assess the role of long non-coding RNA (lncRNA) enolase1-intronic transcript 1 (ENO1-IT1) in Fusobacterium (F.) nucleatum-induced glucose metabolism and colorectal carcinogenesis. RNA immunoprecipitation and chromatin immunoprecipitation sequencing were conducted to identify potential targets of lncRNA ENO1-IT1.ResultsWe have found F. nucleatum abundance correlated with high glucose metabolism in patients with CRC. Furthermore, F. nucleatum supported carcinogenesis via increasing CRC cell glucose metabolism. Mechanistically, F. nucleatum activated lncRNA ENO1-IT1 transcription via upregulating the binding efficiency of transcription factor SP1 to the promoter region of lncRNA ENO1-IT1. Elevated ENO1-IT behaved as a guider modular for KAT7 histone acetyltransferase, specifying the histone modification pattern on its target genes, including ENO1, and consequently altering CRC biological function.Conclusion F. nucleatum and glucose metabolism are mechanistically, biologically and clinically connected to CRC. Targeting ENO1 pathway may be meaningful in treating patients with CRC with elevated F. nucleatum. |
| doi_str_mv | 10.1136/gutjnl-2020-322780 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2580098609</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2580098609</sourcerecordid><originalsourceid>FETCH-LOGICAL-b408t-3fb7e770987b90a063e37f1d9668ce31432c4a6ab9fb0304f7128ae523c06d703</originalsourceid><addsrcrecordid>eNqNkEFLwzAYhoMobk7_gAcJeO78knRNehzD6WBsIPMc0jQdG20yk_Swf29H57yJp_CR532_jwehRwJjQlj2sm3j3tYJBQoJo5QLuEJDkmaim4S4RkMAwpMJT_MBugthDwBC5OQWDRhjRJA0HSI5H2Pb6tqo2DY4Kr81MeDa6o_VFL-u1iRZbAiODh-8a1w0eFsftauPYRewsiV2VrutseY07yzuvpw3Oqoaa2W18ffoplJ1MA_nd4Q-56-b2XuyXL8tZtNlUqQgYsKqghvOIRe8yEFBxgzjFSnzLBPaMJIyqlOVqSKvCmCQVpxQocyEMg1ZyYGN0HPf29351ZoQ5d613nYrJZ0I6IozyDuK9pT2LgRvKnnwu0b5oyQgT05l71SenMreaRd6Ole3RWPKS-RHYgckPVA0-_8Vjn_5y5l_BL4Bd8CPWg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2580098609</pqid></control><display><type>article</type><title>F. nucleatum targets lncRNA ENO1-IT1 to promote glycolysis and oncogenesis in colorectal cancer</title><source>MEDLINE</source><source>PubMed Central</source><creator>Hong, Jie ; Guo, Fangfang ; Lu, Shi-Yuan ; Shen, Chaoqin ; Ma, Dan ; Zhang, Xinyu ; Xie, Yile ; Yan, Tingting ; Yu, TaChung ; Sun, Tiantian ; Qian, Yun ; Zhong, Ming ; Chen, Jinxian ; Peng, Yanshen ; Wang, Cheng ; Zhou, Xiang ; Liu, Jianjun ; Liu, Qiang ; Ma, Xiong ; Chen, Ying-Xuan ; Chen, Haoyan ; Fang, Jing-Yuan</creator><creatorcontrib>Hong, Jie ; Guo, Fangfang ; Lu, Shi-Yuan ; Shen, Chaoqin ; Ma, Dan ; Zhang, Xinyu ; Xie, Yile ; Yan, Tingting ; Yu, TaChung ; Sun, Tiantian ; Qian, Yun ; Zhong, Ming ; Chen, Jinxian ; Peng, Yanshen ; Wang, Cheng ; Zhou, Xiang ; Liu, Jianjun ; Liu, Qiang ; Ma, Xiong ; Chen, Ying-Xuan ; Chen, Haoyan ; Fang, Jing-Yuan</creatorcontrib><description>ObjectiveMicrobiota disorder promotes chronic inflammation and carcinogenesis. High glycolysis is associated with poor prognosis in patients with colorectal cancer (CRC). However, the potential correlation between the gut microbiota and glucose metabolism is unknown in CRC.Design 18F-FDG (18F-fluorodeoxyglucose) PET (positron emission tomography)/CT image scanning data and microbiota PCR analysis were performed to measure the correlation between metabolic alterations and microbiota disorder in 33 patients with CRC. Multiple colorectal cancer models, metabolic analysis and Seahorse assay were established to assess the role of long non-coding RNA (lncRNA) enolase1-intronic transcript 1 (ENO1-IT1) in Fusobacterium (F.) nucleatum-induced glucose metabolism and colorectal carcinogenesis. RNA immunoprecipitation and chromatin immunoprecipitation sequencing were conducted to identify potential targets of lncRNA ENO1-IT1.ResultsWe have found F. nucleatum abundance correlated with high glucose metabolism in patients with CRC. Furthermore, F. nucleatum supported carcinogenesis via increasing CRC cell glucose metabolism. Mechanistically, F. nucleatum activated lncRNA ENO1-IT1 transcription via upregulating the binding efficiency of transcription factor SP1 to the promoter region of lncRNA ENO1-IT1. Elevated ENO1-IT behaved as a guider modular for KAT7 histone acetyltransferase, specifying the histone modification pattern on its target genes, including ENO1, and consequently altering CRC biological function.Conclusion F. nucleatum and glucose metabolism are mechanistically, biologically and clinically connected to CRC. Targeting ENO1 pathway may be meaningful in treating patients with CRC with elevated F. nucleatum.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>DOI: 10.1136/gutjnl-2020-322780</identifier><identifier>PMID: 33318144</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Animals ; Biomarkers, Tumor ; Cancer ; Carcinogenesis ; Carcinogenesis - genetics ; Cell growth ; Chromatin ; Colon ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - diagnostic imaging ; Colorectal Neoplasms - genetics ; DNA-Binding Proteins ; Drug resistance ; Fluorodeoxyglucose F18 - pharmacokinetics ; Fusobacterium Infections - genetics ; Fusobacterium nucleatum ; Gastrointestinal Microbiome ; Gene Expression Regulation, Neoplastic ; Glucose metabolism ; Glycolysis ; Glycolysis - genetics ; Histone acetyltransferase ; Histone Acetyltransferases ; Humans ; Immunoprecipitation ; intestinal bacteria ; Intestinal microflora ; Medical imaging ; Metabolites ; Mice ; Microbiota ; Non-coding RNA ; Patients ; Phosphopyruvate Hydratase ; Positron emission tomography ; Positron Emission Tomography Computed Tomography ; Prognosis ; Radiopharmaceuticals - pharmacokinetics ; RNA, Long Noncoding - genetics ; Signal Transduction ; Sp1 protein ; Tumor Cells, Cultured ; Tumor Suppressor Proteins ; Tumorigenesis</subject><ispartof>Gut, 2021-11, Vol.70 (11), p.2123-2137</ispartof><rights>Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>2021 Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b408t-3fb7e770987b90a063e37f1d9668ce31432c4a6ab9fb0304f7128ae523c06d703</citedby><cites>FETCH-LOGICAL-b408t-3fb7e770987b90a063e37f1d9668ce31432c4a6ab9fb0304f7128ae523c06d703</cites><orcidid>0000-0003-2282-0248 ; 0000-0001-9616-4672 ; 0000-0002-2825-8244 ; 0000-0001-9579-0794 ; 0000-0001-6163-8110</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33318144$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hong, Jie</creatorcontrib><creatorcontrib>Guo, Fangfang</creatorcontrib><creatorcontrib>Lu, Shi-Yuan</creatorcontrib><creatorcontrib>Shen, Chaoqin</creatorcontrib><creatorcontrib>Ma, Dan</creatorcontrib><creatorcontrib>Zhang, Xinyu</creatorcontrib><creatorcontrib>Xie, Yile</creatorcontrib><creatorcontrib>Yan, Tingting</creatorcontrib><creatorcontrib>Yu, TaChung</creatorcontrib><creatorcontrib>Sun, Tiantian</creatorcontrib><creatorcontrib>Qian, Yun</creatorcontrib><creatorcontrib>Zhong, Ming</creatorcontrib><creatorcontrib>Chen, Jinxian</creatorcontrib><creatorcontrib>Peng, Yanshen</creatorcontrib><creatorcontrib>Wang, Cheng</creatorcontrib><creatorcontrib>Zhou, Xiang</creatorcontrib><creatorcontrib>Liu, Jianjun</creatorcontrib><creatorcontrib>Liu, Qiang</creatorcontrib><creatorcontrib>Ma, Xiong</creatorcontrib><creatorcontrib>Chen, Ying-Xuan</creatorcontrib><creatorcontrib>Chen, Haoyan</creatorcontrib><creatorcontrib>Fang, Jing-Yuan</creatorcontrib><title>F. nucleatum targets lncRNA ENO1-IT1 to promote glycolysis and oncogenesis in colorectal cancer</title><title>Gut</title><addtitle>Gut</addtitle><addtitle>Gut</addtitle><description>ObjectiveMicrobiota disorder promotes chronic inflammation and carcinogenesis. High glycolysis is associated with poor prognosis in patients with colorectal cancer (CRC). However, the potential correlation between the gut microbiota and glucose metabolism is unknown in CRC.Design 18F-FDG (18F-fluorodeoxyglucose) PET (positron emission tomography)/CT image scanning data and microbiota PCR analysis were performed to measure the correlation between metabolic alterations and microbiota disorder in 33 patients with CRC. Multiple colorectal cancer models, metabolic analysis and Seahorse assay were established to assess the role of long non-coding RNA (lncRNA) enolase1-intronic transcript 1 (ENO1-IT1) in Fusobacterium (F.) nucleatum-induced glucose metabolism and colorectal carcinogenesis. RNA immunoprecipitation and chromatin immunoprecipitation sequencing were conducted to identify potential targets of lncRNA ENO1-IT1.ResultsWe have found F. nucleatum abundance correlated with high glucose metabolism in patients with CRC. Furthermore, F. nucleatum supported carcinogenesis via increasing CRC cell glucose metabolism. Mechanistically, F. nucleatum activated lncRNA ENO1-IT1 transcription via upregulating the binding efficiency of transcription factor SP1 to the promoter region of lncRNA ENO1-IT1. Elevated ENO1-IT behaved as a guider modular for KAT7 histone acetyltransferase, specifying the histone modification pattern on its target genes, including ENO1, and consequently altering CRC biological function.Conclusion F. nucleatum and glucose metabolism are mechanistically, biologically and clinically connected to CRC. Targeting ENO1 pathway may be meaningful in treating patients with CRC with elevated F. nucleatum.</description><subject>Animals</subject><subject>Biomarkers, Tumor</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Carcinogenesis - genetics</subject><subject>Cell growth</subject><subject>Chromatin</subject><subject>Colon</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - diagnostic imaging</subject><subject>Colorectal Neoplasms - genetics</subject><subject>DNA-Binding Proteins</subject><subject>Drug resistance</subject><subject>Fluorodeoxyglucose F18 - pharmacokinetics</subject><subject>Fusobacterium Infections - genetics</subject><subject>Fusobacterium nucleatum</subject><subject>Gastrointestinal Microbiome</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glucose metabolism</subject><subject>Glycolysis</subject><subject>Glycolysis - genetics</subject><subject>Histone acetyltransferase</subject><subject>Histone Acetyltransferases</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>intestinal bacteria</subject><subject>Intestinal microflora</subject><subject>Medical imaging</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Microbiota</subject><subject>Non-coding RNA</subject><subject>Patients</subject><subject>Phosphopyruvate Hydratase</subject><subject>Positron emission tomography</subject><subject>Positron Emission Tomography Computed Tomography</subject><subject>Prognosis</subject><subject>Radiopharmaceuticals - pharmacokinetics</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Signal Transduction</subject><subject>Sp1 protein</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Proteins</subject><subject>Tumorigenesis</subject><issn>0017-5749</issn><issn>1468-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><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>eNqNkEFLwzAYhoMobk7_gAcJeO78knRNehzD6WBsIPMc0jQdG20yk_Swf29H57yJp_CR532_jwehRwJjQlj2sm3j3tYJBQoJo5QLuEJDkmaim4S4RkMAwpMJT_MBugthDwBC5OQWDRhjRJA0HSI5H2Pb6tqo2DY4Kr81MeDa6o_VFL-u1iRZbAiODh-8a1w0eFsftauPYRewsiV2VrutseY07yzuvpw3Oqoaa2W18ffoplJ1MA_nd4Q-56-b2XuyXL8tZtNlUqQgYsKqghvOIRe8yEFBxgzjFSnzLBPaMJIyqlOVqSKvCmCQVpxQocyEMg1ZyYGN0HPf29351ZoQ5d613nYrJZ0I6IozyDuK9pT2LgRvKnnwu0b5oyQgT05l71SenMreaRd6Ole3RWPKS-RHYgckPVA0-_8Vjn_5y5l_BL4Bd8CPWg</recordid><startdate>20211101</startdate><enddate>20211101</enddate><creator>Hong, Jie</creator><creator>Guo, Fangfang</creator><creator>Lu, Shi-Yuan</creator><creator>Shen, Chaoqin</creator><creator>Ma, Dan</creator><creator>Zhang, Xinyu</creator><creator>Xie, Yile</creator><creator>Yan, Tingting</creator><creator>Yu, TaChung</creator><creator>Sun, Tiantian</creator><creator>Qian, Yun</creator><creator>Zhong, Ming</creator><creator>Chen, Jinxian</creator><creator>Peng, Yanshen</creator><creator>Wang, Cheng</creator><creator>Zhou, Xiang</creator><creator>Liu, Jianjun</creator><creator>Liu, Qiang</creator><creator>Ma, Xiong</creator><creator>Chen, Ying-Xuan</creator><creator>Chen, Haoyan</creator><creator>Fang, Jing-Yuan</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ Publishing Group LTD</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>88I</scope><scope>8AF</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>BTHHO</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>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0003-2282-0248</orcidid><orcidid>https://orcid.org/0000-0001-9616-4672</orcidid><orcidid>https://orcid.org/0000-0002-2825-8244</orcidid><orcidid>https://orcid.org/0000-0001-9579-0794</orcidid><orcidid>https://orcid.org/0000-0001-6163-8110</orcidid></search><sort><creationdate>20211101</creationdate><title>F. nucleatum targets lncRNA ENO1-IT1 to promote glycolysis and oncogenesis in colorectal cancer</title><author>Hong, Jie ; Guo, Fangfang ; Lu, Shi-Yuan ; Shen, Chaoqin ; Ma, Dan ; Zhang, Xinyu ; Xie, Yile ; Yan, Tingting ; Yu, TaChung ; Sun, Tiantian ; Qian, Yun ; Zhong, Ming ; Chen, Jinxian ; Peng, Yanshen ; Wang, Cheng ; Zhou, Xiang ; Liu, Jianjun ; Liu, Qiang ; Ma, Xiong ; Chen, Ying-Xuan ; Chen, Haoyan ; Fang, Jing-Yuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b408t-3fb7e770987b90a063e37f1d9668ce31432c4a6ab9fb0304f7128ae523c06d703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Biomarkers, Tumor</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Carcinogenesis - genetics</topic><topic>Cell growth</topic><topic>Chromatin</topic><topic>Colon</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - diagnostic imaging</topic><topic>Colorectal Neoplasms - genetics</topic><topic>DNA-Binding Proteins</topic><topic>Drug resistance</topic><topic>Fluorodeoxyglucose F18 - pharmacokinetics</topic><topic>Fusobacterium Infections - genetics</topic><topic>Fusobacterium nucleatum</topic><topic>Gastrointestinal Microbiome</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glucose metabolism</topic><topic>Glycolysis</topic><topic>Glycolysis - genetics</topic><topic>Histone acetyltransferase</topic><topic>Histone Acetyltransferases</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>intestinal bacteria</topic><topic>Intestinal microflora</topic><topic>Medical imaging</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Microbiota</topic><topic>Non-coding RNA</topic><topic>Patients</topic><topic>Phosphopyruvate Hydratase</topic><topic>Positron emission tomography</topic><topic>Positron Emission Tomography Computed Tomography</topic><topic>Prognosis</topic><topic>Radiopharmaceuticals - pharmacokinetics</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Signal Transduction</topic><topic>Sp1 protein</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Suppressor Proteins</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hong, Jie</creatorcontrib><creatorcontrib>Guo, Fangfang</creatorcontrib><creatorcontrib>Lu, Shi-Yuan</creatorcontrib><creatorcontrib>Shen, Chaoqin</creatorcontrib><creatorcontrib>Ma, Dan</creatorcontrib><creatorcontrib>Zhang, Xinyu</creatorcontrib><creatorcontrib>Xie, Yile</creatorcontrib><creatorcontrib>Yan, Tingting</creatorcontrib><creatorcontrib>Yu, TaChung</creatorcontrib><creatorcontrib>Sun, Tiantian</creatorcontrib><creatorcontrib>Qian, Yun</creatorcontrib><creatorcontrib>Zhong, Ming</creatorcontrib><creatorcontrib>Chen, Jinxian</creatorcontrib><creatorcontrib>Peng, Yanshen</creatorcontrib><creatorcontrib>Wang, Cheng</creatorcontrib><creatorcontrib>Zhou, Xiang</creatorcontrib><creatorcontrib>Liu, Jianjun</creatorcontrib><creatorcontrib>Liu, Qiang</creatorcontrib><creatorcontrib>Ma, Xiong</creatorcontrib><creatorcontrib>Chen, Ying-Xuan</creatorcontrib><creatorcontrib>Chen, Haoyan</creatorcontrib><creatorcontrib>Fang, Jing-Yuan</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>Science Database (Alumni Edition)</collection><collection>STEM 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>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 (ProQuest)</collection><collection>BMJ Journals</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>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science 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><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hong, Jie</au><au>Guo, Fangfang</au><au>Lu, Shi-Yuan</au><au>Shen, Chaoqin</au><au>Ma, Dan</au><au>Zhang, Xinyu</au><au>Xie, Yile</au><au>Yan, Tingting</au><au>Yu, TaChung</au><au>Sun, Tiantian</au><au>Qian, Yun</au><au>Zhong, Ming</au><au>Chen, Jinxian</au><au>Peng, Yanshen</au><au>Wang, Cheng</au><au>Zhou, Xiang</au><au>Liu, Jianjun</au><au>Liu, Qiang</au><au>Ma, Xiong</au><au>Chen, Ying-Xuan</au><au>Chen, Haoyan</au><au>Fang, Jing-Yuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>F. nucleatum targets lncRNA ENO1-IT1 to promote glycolysis and oncogenesis in colorectal cancer</atitle><jtitle>Gut</jtitle><stitle>Gut</stitle><addtitle>Gut</addtitle><date>2021-11-01</date><risdate>2021</risdate><volume>70</volume><issue>11</issue><spage>2123</spage><epage>2137</epage><pages>2123-2137</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><abstract>ObjectiveMicrobiota disorder promotes chronic inflammation and carcinogenesis. High glycolysis is associated with poor prognosis in patients with colorectal cancer (CRC). However, the potential correlation between the gut microbiota and glucose metabolism is unknown in CRC.Design 18F-FDG (18F-fluorodeoxyglucose) PET (positron emission tomography)/CT image scanning data and microbiota PCR analysis were performed to measure the correlation between metabolic alterations and microbiota disorder in 33 patients with CRC. Multiple colorectal cancer models, metabolic analysis and Seahorse assay were established to assess the role of long non-coding RNA (lncRNA) enolase1-intronic transcript 1 (ENO1-IT1) in Fusobacterium (F.) nucleatum-induced glucose metabolism and colorectal carcinogenesis. RNA immunoprecipitation and chromatin immunoprecipitation sequencing were conducted to identify potential targets of lncRNA ENO1-IT1.ResultsWe have found F. nucleatum abundance correlated with high glucose metabolism in patients with CRC. Furthermore, F. nucleatum supported carcinogenesis via increasing CRC cell glucose metabolism. Mechanistically, F. nucleatum activated lncRNA ENO1-IT1 transcription via upregulating the binding efficiency of transcription factor SP1 to the promoter region of lncRNA ENO1-IT1. Elevated ENO1-IT behaved as a guider modular for KAT7 histone acetyltransferase, specifying the histone modification pattern on its target genes, including ENO1, and consequently altering CRC biological function.Conclusion F. nucleatum and glucose metabolism are mechanistically, biologically and clinically connected to CRC. Targeting ENO1 pathway may be meaningful in treating patients with CRC with elevated F. nucleatum.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>33318144</pmid><doi>10.1136/gutjnl-2020-322780</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-2282-0248</orcidid><orcidid>https://orcid.org/0000-0001-9616-4672</orcidid><orcidid>https://orcid.org/0000-0002-2825-8244</orcidid><orcidid>https://orcid.org/0000-0001-9579-0794</orcidid><orcidid>https://orcid.org/0000-0001-6163-8110</orcidid></addata></record> |
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| subjects | Animals Biomarkers, Tumor Cancer Carcinogenesis Carcinogenesis - genetics Cell growth Chromatin Colon Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - diagnostic imaging Colorectal Neoplasms - genetics DNA-Binding Proteins Drug resistance Fluorodeoxyglucose F18 - pharmacokinetics Fusobacterium Infections - genetics Fusobacterium nucleatum Gastrointestinal Microbiome Gene Expression Regulation, Neoplastic Glucose metabolism Glycolysis Glycolysis - genetics Histone acetyltransferase Histone Acetyltransferases Humans Immunoprecipitation intestinal bacteria Intestinal microflora Medical imaging Metabolites Mice Microbiota Non-coding RNA Patients Phosphopyruvate Hydratase Positron emission tomography Positron Emission Tomography Computed Tomography Prognosis Radiopharmaceuticals - pharmacokinetics RNA, Long Noncoding - genetics Signal Transduction Sp1 protein Tumor Cells, Cultured Tumor Suppressor Proteins Tumorigenesis |
| title | F. nucleatum targets lncRNA ENO1-IT1 to promote glycolysis and oncogenesis in colorectal cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-24T02%3A42%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=F.%20nucleatum%20targets%20lncRNA%20ENO1-IT1%20to%20promote%20glycolysis%20and%20oncogenesis%20in%20colorectal%20cancer&rft.jtitle=Gut&rft.au=Hong,%20Jie&rft.date=2021-11-01&rft.volume=70&rft.issue=11&rft.spage=2123&rft.epage=2137&rft.pages=2123-2137&rft.issn=0017-5749&rft.eissn=1468-3288&rft_id=info:doi/10.1136/gutjnl-2020-322780&rft_dat=%3Cproquest_cross%3E2580098609%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2580098609&rft_id=info:pmid/33318144&rfr_iscdi=true |