CSTF2 mediated mRNA N 6 -methyladenosine modification drives pancreatic ductal adenocarcinoma m 6 A subtypes
N -methyladenosine (m A) modification of gene transcripts plays critical roles in cancer. Here we report transcriptomic m A profiling in 98 tissue samples from 65 individuals with pancreatic ductal adenocarcinoma (PDAC). We identify 17,996 m A peaks with 195 hyper-methylated and 93 hypo-methylated i...
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| Veröffentlicht in: | Nature communications 2023-10, Vol.14 (1), p.6334 |
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| creator | Zheng, Yanfen Li, Xingyang Deng, Shuang Zhao, Hongzhe Ye, Ying Zhang, Shaoping Huang, Xudong Bai, Ruihong Zhuang, Lisha Zhou, Quanbo Li, Mei Su, Jiachun Li, Rui Bao, Xiaoqiong Zeng, Lingxing Chen, Rufu Zheng, Jian Lin, Dongxin He, Chuan Zhang, Jialiang Zuo, Zhixiang |
| description | N
-methyladenosine (m
A) modification of gene transcripts plays critical roles in cancer. Here we report transcriptomic m
A profiling in 98 tissue samples from 65 individuals with pancreatic ductal adenocarcinoma (PDAC). We identify 17,996 m
A peaks with 195 hyper-methylated and 93 hypo-methylated in PDAC compared with adjacent normal tissues. The differential m
A modifications distinguish two PDAC subtypes with different prognosis outcomes. The formation of the two subtypes is driven by a newly identified m
A regulator CSTF2 that co-transcriptionally regulates m
A installation through slowing the RNA Pol II elongation rate during gene transcription. We find that most of the CSTF2-regulated m
As have positive effects on the RNA level of host genes, and CSTF2-regulated m
As are mainly recognized by IGF2BP2, an m
A reader that stabilizes mRNAs. These results provide a promising PDAC subtyping strategy and potential therapeutic targets for precision medicine of PDAC. |
| doi_str_mv | 10.1038/s41467-023-41861-y |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed</sourceid><recordid>TN_cdi_pubmed_primary_37816727</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>37816727</sourcerecordid><originalsourceid>FETCH-pubmed_primary_378167273</originalsourceid><addsrcrecordid>eNqFjs1KAzEUhUNBbNG-gItyXyCaPybTZSkWV11o9-U2ucXIJDMkmcK8vYPo2rM5cPg4fIw9SfEshW5fipGmsVwozY1sG8mnBVspYSSXVuklW5fyJeborWyNuWdLbVvZWGVXrNt_nA4KIvmAlTzE9-MOjtAAj1Q_pw49pb6ERBB7H67BYQ19Ap_DjQoMmFymeXLgR1exgx_eYXYh9REhzk87KOOlTgOVR3Z3xa7Q-rcf2Obwetq_8WG8zAbnIYeIeTr_6el_gW_OWUvZ</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>CSTF2 mediated mRNA N 6 -methyladenosine modification drives pancreatic ductal adenocarcinoma m 6 A subtypes</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Springer Nature OA Free Journals</source><source>Nature Free</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Zheng, Yanfen ; Li, Xingyang ; Deng, Shuang ; Zhao, Hongzhe ; Ye, Ying ; Zhang, Shaoping ; Huang, Xudong ; Bai, Ruihong ; Zhuang, Lisha ; Zhou, Quanbo ; Li, Mei ; Su, Jiachun ; Li, Rui ; Bao, Xiaoqiong ; Zeng, Lingxing ; Chen, Rufu ; Zheng, Jian ; Lin, Dongxin ; He, Chuan ; Zhang, Jialiang ; Zuo, Zhixiang</creator><creatorcontrib>Zheng, Yanfen ; Li, Xingyang ; Deng, Shuang ; Zhao, Hongzhe ; Ye, Ying ; Zhang, Shaoping ; Huang, Xudong ; Bai, Ruihong ; Zhuang, Lisha ; Zhou, Quanbo ; Li, Mei ; Su, Jiachun ; Li, Rui ; Bao, Xiaoqiong ; Zeng, Lingxing ; Chen, Rufu ; Zheng, Jian ; Lin, Dongxin ; He, Chuan ; Zhang, Jialiang ; Zuo, Zhixiang</creatorcontrib><description>N
-methyladenosine (m
A) modification of gene transcripts plays critical roles in cancer. Here we report transcriptomic m
A profiling in 98 tissue samples from 65 individuals with pancreatic ductal adenocarcinoma (PDAC). We identify 17,996 m
A peaks with 195 hyper-methylated and 93 hypo-methylated in PDAC compared with adjacent normal tissues. The differential m
A modifications distinguish two PDAC subtypes with different prognosis outcomes. The formation of the two subtypes is driven by a newly identified m
A regulator CSTF2 that co-transcriptionally regulates m
A installation through slowing the RNA Pol II elongation rate during gene transcription. We find that most of the CSTF2-regulated m
As have positive effects on the RNA level of host genes, and CSTF2-regulated m
As are mainly recognized by IGF2BP2, an m
A reader that stabilizes mRNAs. These results provide a promising PDAC subtyping strategy and potential therapeutic targets for precision medicine of PDAC.</description><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/s41467-023-41861-y</identifier><identifier>PMID: 37816727</identifier><language>eng</language><publisher>England</publisher><subject>Carcinoma, Pancreatic Ductal - pathology ; Gene Expression Regulation, Neoplastic ; Humans ; Pancreatic Neoplasms - pathology ; RNA, Messenger - genetics ; RNA-Binding Proteins - genetics</subject><ispartof>Nature communications, 2023-10, Vol.14 (1), p.6334</ispartof><rights>2023. Springer Nature Limited.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0003-4319-7424 ; 0000-0001-9554-063X ; 0000-0003-1626-6674 ; 0000-0002-0846-8762 ; 0000-0002-2492-2689 ; 0000-0001-9831-7038 ; 0000-0002-8445-4901</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,862,27907,27908</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37816727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Yanfen</creatorcontrib><creatorcontrib>Li, Xingyang</creatorcontrib><creatorcontrib>Deng, Shuang</creatorcontrib><creatorcontrib>Zhao, Hongzhe</creatorcontrib><creatorcontrib>Ye, Ying</creatorcontrib><creatorcontrib>Zhang, Shaoping</creatorcontrib><creatorcontrib>Huang, Xudong</creatorcontrib><creatorcontrib>Bai, Ruihong</creatorcontrib><creatorcontrib>Zhuang, Lisha</creatorcontrib><creatorcontrib>Zhou, Quanbo</creatorcontrib><creatorcontrib>Li, Mei</creatorcontrib><creatorcontrib>Su, Jiachun</creatorcontrib><creatorcontrib>Li, Rui</creatorcontrib><creatorcontrib>Bao, Xiaoqiong</creatorcontrib><creatorcontrib>Zeng, Lingxing</creatorcontrib><creatorcontrib>Chen, Rufu</creatorcontrib><creatorcontrib>Zheng, Jian</creatorcontrib><creatorcontrib>Lin, Dongxin</creatorcontrib><creatorcontrib>He, Chuan</creatorcontrib><creatorcontrib>Zhang, Jialiang</creatorcontrib><creatorcontrib>Zuo, Zhixiang</creatorcontrib><title>CSTF2 mediated mRNA N 6 -methyladenosine modification drives pancreatic ductal adenocarcinoma m 6 A subtypes</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><description>N
-methyladenosine (m
A) modification of gene transcripts plays critical roles in cancer. Here we report transcriptomic m
A profiling in 98 tissue samples from 65 individuals with pancreatic ductal adenocarcinoma (PDAC). We identify 17,996 m
A peaks with 195 hyper-methylated and 93 hypo-methylated in PDAC compared with adjacent normal tissues. The differential m
A modifications distinguish two PDAC subtypes with different prognosis outcomes. The formation of the two subtypes is driven by a newly identified m
A regulator CSTF2 that co-transcriptionally regulates m
A installation through slowing the RNA Pol II elongation rate during gene transcription. We find that most of the CSTF2-regulated m
As have positive effects on the RNA level of host genes, and CSTF2-regulated m
As are mainly recognized by IGF2BP2, an m
A reader that stabilizes mRNAs. These results provide a promising PDAC subtyping strategy and potential therapeutic targets for precision medicine of PDAC.</description><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA-Binding Proteins - genetics</subject><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjs1KAzEUhUNBbNG-gItyXyCaPybTZSkWV11o9-U2ucXIJDMkmcK8vYPo2rM5cPg4fIw9SfEshW5fipGmsVwozY1sG8mnBVspYSSXVuklW5fyJeborWyNuWdLbVvZWGVXrNt_nA4KIvmAlTzE9-MOjtAAj1Q_pw49pb6ERBB7H67BYQ19Ap_DjQoMmFymeXLgR1exgx_eYXYh9REhzk87KOOlTgOVR3Z3xa7Q-rcf2Obwetq_8WG8zAbnIYeIeTr_6el_gW_OWUvZ</recordid><startdate>20231010</startdate><enddate>20231010</enddate><creator>Zheng, Yanfen</creator><creator>Li, Xingyang</creator><creator>Deng, Shuang</creator><creator>Zhao, Hongzhe</creator><creator>Ye, Ying</creator><creator>Zhang, Shaoping</creator><creator>Huang, Xudong</creator><creator>Bai, Ruihong</creator><creator>Zhuang, Lisha</creator><creator>Zhou, Quanbo</creator><creator>Li, Mei</creator><creator>Su, Jiachun</creator><creator>Li, Rui</creator><creator>Bao, Xiaoqiong</creator><creator>Zeng, Lingxing</creator><creator>Chen, Rufu</creator><creator>Zheng, Jian</creator><creator>Lin, Dongxin</creator><creator>He, Chuan</creator><creator>Zhang, Jialiang</creator><creator>Zuo, Zhixiang</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><orcidid>https://orcid.org/0000-0003-4319-7424</orcidid><orcidid>https://orcid.org/0000-0001-9554-063X</orcidid><orcidid>https://orcid.org/0000-0003-1626-6674</orcidid><orcidid>https://orcid.org/0000-0002-0846-8762</orcidid><orcidid>https://orcid.org/0000-0002-2492-2689</orcidid><orcidid>https://orcid.org/0000-0001-9831-7038</orcidid><orcidid>https://orcid.org/0000-0002-8445-4901</orcidid></search><sort><creationdate>20231010</creationdate><title>CSTF2 mediated mRNA N 6 -methyladenosine modification drives pancreatic ductal adenocarcinoma m 6 A subtypes</title><author>Zheng, Yanfen ; Li, Xingyang ; Deng, Shuang ; Zhao, Hongzhe ; Ye, Ying ; Zhang, Shaoping ; Huang, Xudong ; Bai, Ruihong ; Zhuang, Lisha ; Zhou, Quanbo ; Li, Mei ; Su, Jiachun ; Li, Rui ; Bao, Xiaoqiong ; Zeng, Lingxing ; Chen, Rufu ; Zheng, Jian ; Lin, Dongxin ; He, Chuan ; Zhang, Jialiang ; Zuo, Zhixiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_378167273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA-Binding Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Yanfen</creatorcontrib><creatorcontrib>Li, Xingyang</creatorcontrib><creatorcontrib>Deng, Shuang</creatorcontrib><creatorcontrib>Zhao, Hongzhe</creatorcontrib><creatorcontrib>Ye, Ying</creatorcontrib><creatorcontrib>Zhang, Shaoping</creatorcontrib><creatorcontrib>Huang, Xudong</creatorcontrib><creatorcontrib>Bai, Ruihong</creatorcontrib><creatorcontrib>Zhuang, Lisha</creatorcontrib><creatorcontrib>Zhou, Quanbo</creatorcontrib><creatorcontrib>Li, Mei</creatorcontrib><creatorcontrib>Su, Jiachun</creatorcontrib><creatorcontrib>Li, Rui</creatorcontrib><creatorcontrib>Bao, Xiaoqiong</creatorcontrib><creatorcontrib>Zeng, Lingxing</creatorcontrib><creatorcontrib>Chen, Rufu</creatorcontrib><creatorcontrib>Zheng, Jian</creatorcontrib><creatorcontrib>Lin, Dongxin</creatorcontrib><creatorcontrib>He, Chuan</creatorcontrib><creatorcontrib>Zhang, Jialiang</creatorcontrib><creatorcontrib>Zuo, Zhixiang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Yanfen</au><au>Li, Xingyang</au><au>Deng, Shuang</au><au>Zhao, Hongzhe</au><au>Ye, Ying</au><au>Zhang, Shaoping</au><au>Huang, Xudong</au><au>Bai, Ruihong</au><au>Zhuang, Lisha</au><au>Zhou, Quanbo</au><au>Li, Mei</au><au>Su, Jiachun</au><au>Li, Rui</au><au>Bao, Xiaoqiong</au><au>Zeng, Lingxing</au><au>Chen, Rufu</au><au>Zheng, Jian</au><au>Lin, Dongxin</au><au>He, Chuan</au><au>Zhang, Jialiang</au><au>Zuo, Zhixiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CSTF2 mediated mRNA N 6 -methyladenosine modification drives pancreatic ductal adenocarcinoma m 6 A subtypes</atitle><jtitle>Nature communications</jtitle><addtitle>Nat Commun</addtitle><date>2023-10-10</date><risdate>2023</risdate><volume>14</volume><issue>1</issue><spage>6334</spage><pages>6334-</pages><eissn>2041-1723</eissn><abstract>N
-methyladenosine (m
A) modification of gene transcripts plays critical roles in cancer. Here we report transcriptomic m
A profiling in 98 tissue samples from 65 individuals with pancreatic ductal adenocarcinoma (PDAC). We identify 17,996 m
A peaks with 195 hyper-methylated and 93 hypo-methylated in PDAC compared with adjacent normal tissues. The differential m
A modifications distinguish two PDAC subtypes with different prognosis outcomes. The formation of the two subtypes is driven by a newly identified m
A regulator CSTF2 that co-transcriptionally regulates m
A installation through slowing the RNA Pol II elongation rate during gene transcription. We find that most of the CSTF2-regulated m
As have positive effects on the RNA level of host genes, and CSTF2-regulated m
As are mainly recognized by IGF2BP2, an m
A reader that stabilizes mRNAs. These results provide a promising PDAC subtyping strategy and potential therapeutic targets for precision medicine of PDAC.</abstract><cop>England</cop><pmid>37816727</pmid><doi>10.1038/s41467-023-41861-y</doi><orcidid>https://orcid.org/0000-0003-4319-7424</orcidid><orcidid>https://orcid.org/0000-0001-9554-063X</orcidid><orcidid>https://orcid.org/0000-0003-1626-6674</orcidid><orcidid>https://orcid.org/0000-0002-0846-8762</orcidid><orcidid>https://orcid.org/0000-0002-2492-2689</orcidid><orcidid>https://orcid.org/0000-0001-9831-7038</orcidid><orcidid>https://orcid.org/0000-0002-8445-4901</orcidid></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Carcinoma, Pancreatic Ductal - pathology Gene Expression Regulation, Neoplastic Humans Pancreatic Neoplasms - pathology RNA, Messenger - genetics RNA-Binding Proteins - genetics |
| title | CSTF2 mediated mRNA N 6 -methyladenosine modification drives pancreatic ductal adenocarcinoma m 6 A subtypes |
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