Fusobacterium nucleatum induces excess methyltransferase‐like 3‐mediated microRNA‐4717‐3p maturation to promote colorectal cancer cell proliferation
Fusobacterium nucleatum infection plays vital roles in colorectal cancer (CRC) progression. Overexpression of microRNA‐4717‐3p (miR‐4717) was reported to be upregulated in F. nucleatum positive CRC tissues, however, the underlying mechanism is unknown. In this study, we found that miR‐4717 promoted...
Gespeichert in:
| Veröffentlicht in: | Cancer science 2022-11, Vol.113 (11), p.3787-3800 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 3800 |
|---|---|
| container_issue | 11 |
| container_start_page | 3787 |
| container_title | Cancer science |
| container_volume | 113 |
| creator | Xu, Qiaolin Lu, Xiaoxue Li, Jing Feng, Yuyang Tang, Jie Zhang, Tao Mao, Yilan Lan, Yuanzhi Luo, Huaxing Zeng, Linghai Xiang, Yuanyuan Hu, Lv Zhang, Yan Li, Qian Deng, Ling He, Xiaoyi Tang, Bin Mao, Xuhu Zeng, Dongzhu |
| description | Fusobacterium nucleatum infection plays vital roles in colorectal cancer (CRC) progression. Overexpression of microRNA‐4717‐3p (miR‐4717) was reported to be upregulated in F. nucleatum positive CRC tissues, however, the underlying mechanism is unknown. In this study, we found that miR‐4717 promoted CRC cell proliferation in vitro and growth of CRC in vivo following F. nucleatum infection. MicroRNA‐4717 suppressed the expression of mitogen‐activated protein kinase kinase 4 (MAP2K4), a tumor suppressor, by directly targeting its 3′‐UTR. Furthermore, we confirmed that methyltransferase‐like 3 (METTL3)‐dependent m6A methylation could methylate primary (pri)‐miR‐4717, which further promoted the maturation of pri‐miR‐4717, and METTL3 positively regulated CRC cell proliferation through miR‐4717/MAP2K4 pathways. In conclusion, F. nucleatum‐induced miR‐4717 excessive maturation through METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC.
F. nucleatum‐induced miR‐4717 excessive maturation via METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC. |
| doi_str_mv | 10.1111/cas.15536 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9633291</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2704869274</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4446-f9c3fc2915de39c8c78b960b6efb3c7837789a306750d2b4a344d5afdb962f03</originalsourceid><addsrcrecordid>eNp1kcFuFSEUhonR2PbqwjcgcaOLaZmBgWFjcnNjq0mjiXZPGOaMpTLDFZjq3fkIPoBP55N4bm9jooksOAf4-A8_h5BnNTutcZw5m0_rtuXyATmuudCVYkw-vMtVpRlvjshJzjeMcSm0eEyOeKs7IbU-Jj_Plxx76wokv0x0XlwAWzDz87A4yBS-4ZzpBOV6F0qycx4h2Qy_vv8I_jNQjskEg7cFBjp5l-KHd2vcE6pWGPiWTqiXbPFxpiXSbYpTLEBdDDGBKzZQZ2cHiToIYX8c_L7Cnn9CHo02ZHh6H1fk6vz11eZNdfn-4u1mfVk5IYSsRu346BpdtwNw7Tqnul5L1ksYe44LrlSnLWdStWxoemG5EENrxwGpZmR8RV4dZLdLj1YczOgzmG3yk007E603f5_M_tp8irdGS86xLAq8uBdI8csCuZjJ570dO0NcsmkUE53UjRKIPv8HvYlLmtEdUrxutewwrsjLA4XfmXOC8c9jamb2LTfYcnPXcmTPDuxXH2D3f9Bs1h8PN34DAPGz6A</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2731596827</pqid></control><display><type>article</type><title>Fusobacterium nucleatum induces excess methyltransferase‐like 3‐mediated microRNA‐4717‐3p maturation to promote colorectal cancer cell proliferation</title><source>DOAJ Directory of Open Access Journals</source><source>Access via Wiley Online Library</source><source>Wiley Online Library Open Access</source><source>PubMed Central</source><creator>Xu, Qiaolin ; Lu, Xiaoxue ; Li, Jing ; Feng, Yuyang ; Tang, Jie ; Zhang, Tao ; Mao, Yilan ; Lan, Yuanzhi ; Luo, Huaxing ; Zeng, Linghai ; Xiang, Yuanyuan ; Hu, Lv ; Zhang, Yan ; Li, Qian ; Deng, Ling ; He, Xiaoyi ; Tang, Bin ; Mao, Xuhu ; Zeng, Dongzhu</creator><creatorcontrib>Xu, Qiaolin ; Lu, Xiaoxue ; Li, Jing ; Feng, Yuyang ; Tang, Jie ; Zhang, Tao ; Mao, Yilan ; Lan, Yuanzhi ; Luo, Huaxing ; Zeng, Linghai ; Xiang, Yuanyuan ; Hu, Lv ; Zhang, Yan ; Li, Qian ; Deng, Ling ; He, Xiaoyi ; Tang, Bin ; Mao, Xuhu ; Zeng, Dongzhu</creatorcontrib><description>Fusobacterium nucleatum infection plays vital roles in colorectal cancer (CRC) progression. Overexpression of microRNA‐4717‐3p (miR‐4717) was reported to be upregulated in F. nucleatum positive CRC tissues, however, the underlying mechanism is unknown. In this study, we found that miR‐4717 promoted CRC cell proliferation in vitro and growth of CRC in vivo following F. nucleatum infection. MicroRNA‐4717 suppressed the expression of mitogen‐activated protein kinase kinase 4 (MAP2K4), a tumor suppressor, by directly targeting its 3′‐UTR. Furthermore, we confirmed that methyltransferase‐like 3 (METTL3)‐dependent m6A methylation could methylate primary (pri)‐miR‐4717, which further promoted the maturation of pri‐miR‐4717, and METTL3 positively regulated CRC cell proliferation through miR‐4717/MAP2K4 pathways. In conclusion, F. nucleatum‐induced miR‐4717 excessive maturation through METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC.
F. nucleatum‐induced miR‐4717 excessive maturation via METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.15536</identifier><identifier>PMID: 35984699</identifier><language>eng</language><publisher>Tokyo: John Wiley & Sons, Inc</publisher><subject>3' Untranslated regions ; Biotechnology ; Cell cycle ; Cell growth ; Cell proliferation ; Colorectal cancer ; Colorectal carcinoma ; Epigenetics ; Fusobacterium nucleatum ; Gene expression ; Infections ; Kinases ; Laboratory animals ; MAP2K4 ; Maturation ; Methylation ; Methyltransferase ; METTL3 ; MicroRNAs ; miRNA ; miR‐4717‐3p ; N6-methyladenosine ; Original ; Pathogens ; Protein kinase ; Proteins ; Reagents ; Therapeutic targets ; Tumor suppressor genes ; Tumors</subject><ispartof>Cancer science, 2022-11, Vol.113 (11), p.3787-3800</ispartof><rights>2022 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by-nc-nd/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-c4446-f9c3fc2915de39c8c78b960b6efb3c7837789a306750d2b4a344d5afdb962f03</citedby><cites>FETCH-LOGICAL-c4446-f9c3fc2915de39c8c78b960b6efb3c7837789a306750d2b4a344d5afdb962f03</cites><orcidid>0000-0003-3540-0728</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9633291/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9633291/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids></links><search><creatorcontrib>Xu, Qiaolin</creatorcontrib><creatorcontrib>Lu, Xiaoxue</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Feng, Yuyang</creatorcontrib><creatorcontrib>Tang, Jie</creatorcontrib><creatorcontrib>Zhang, Tao</creatorcontrib><creatorcontrib>Mao, Yilan</creatorcontrib><creatorcontrib>Lan, Yuanzhi</creatorcontrib><creatorcontrib>Luo, Huaxing</creatorcontrib><creatorcontrib>Zeng, Linghai</creatorcontrib><creatorcontrib>Xiang, Yuanyuan</creatorcontrib><creatorcontrib>Hu, Lv</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Deng, Ling</creatorcontrib><creatorcontrib>He, Xiaoyi</creatorcontrib><creatorcontrib>Tang, Bin</creatorcontrib><creatorcontrib>Mao, Xuhu</creatorcontrib><creatorcontrib>Zeng, Dongzhu</creatorcontrib><title>Fusobacterium nucleatum induces excess methyltransferase‐like 3‐mediated microRNA‐4717‐3p maturation to promote colorectal cancer cell proliferation</title><title>Cancer science</title><description>Fusobacterium nucleatum infection plays vital roles in colorectal cancer (CRC) progression. Overexpression of microRNA‐4717‐3p (miR‐4717) was reported to be upregulated in F. nucleatum positive CRC tissues, however, the underlying mechanism is unknown. In this study, we found that miR‐4717 promoted CRC cell proliferation in vitro and growth of CRC in vivo following F. nucleatum infection. MicroRNA‐4717 suppressed the expression of mitogen‐activated protein kinase kinase 4 (MAP2K4), a tumor suppressor, by directly targeting its 3′‐UTR. Furthermore, we confirmed that methyltransferase‐like 3 (METTL3)‐dependent m6A methylation could methylate primary (pri)‐miR‐4717, which further promoted the maturation of pri‐miR‐4717, and METTL3 positively regulated CRC cell proliferation through miR‐4717/MAP2K4 pathways. In conclusion, F. nucleatum‐induced miR‐4717 excessive maturation through METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC.
F. nucleatum‐induced miR‐4717 excessive maturation via METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC.</description><subject>3' Untranslated regions</subject><subject>Biotechnology</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Epigenetics</subject><subject>Fusobacterium nucleatum</subject><subject>Gene expression</subject><subject>Infections</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>MAP2K4</subject><subject>Maturation</subject><subject>Methylation</subject><subject>Methyltransferase</subject><subject>METTL3</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>miR‐4717‐3p</subject><subject>N6-methyladenosine</subject><subject>Original</subject><subject>Pathogens</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Reagents</subject><subject>Therapeutic targets</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kcFuFSEUhonR2PbqwjcgcaOLaZmBgWFjcnNjq0mjiXZPGOaMpTLDFZjq3fkIPoBP55N4bm9jooksOAf4-A8_h5BnNTutcZw5m0_rtuXyATmuudCVYkw-vMtVpRlvjshJzjeMcSm0eEyOeKs7IbU-Jj_Plxx76wokv0x0XlwAWzDz87A4yBS-4ZzpBOV6F0qycx4h2Qy_vv8I_jNQjskEg7cFBjp5l-KHd2vcE6pWGPiWTqiXbPFxpiXSbYpTLEBdDDGBKzZQZ2cHiToIYX8c_L7Cnn9CHo02ZHh6H1fk6vz11eZNdfn-4u1mfVk5IYSsRu346BpdtwNw7Tqnul5L1ksYe44LrlSnLWdStWxoemG5EENrxwGpZmR8RV4dZLdLj1YczOgzmG3yk007E603f5_M_tp8irdGS86xLAq8uBdI8csCuZjJ570dO0NcsmkUE53UjRKIPv8HvYlLmtEdUrxutewwrsjLA4XfmXOC8c9jamb2LTfYcnPXcmTPDuxXH2D3f9Bs1h8PN34DAPGz6A</recordid><startdate>202211</startdate><enddate>202211</enddate><creator>Xu, Qiaolin</creator><creator>Lu, Xiaoxue</creator><creator>Li, Jing</creator><creator>Feng, Yuyang</creator><creator>Tang, Jie</creator><creator>Zhang, Tao</creator><creator>Mao, Yilan</creator><creator>Lan, Yuanzhi</creator><creator>Luo, Huaxing</creator><creator>Zeng, Linghai</creator><creator>Xiang, Yuanyuan</creator><creator>Hu, Lv</creator><creator>Zhang, Yan</creator><creator>Li, Qian</creator><creator>Deng, Ling</creator><creator>He, Xiaoyi</creator><creator>Tang, Bin</creator><creator>Mao, Xuhu</creator><creator>Zeng, Dongzhu</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3540-0728</orcidid></search><sort><creationdate>202211</creationdate><title>Fusobacterium nucleatum induces excess methyltransferase‐like 3‐mediated microRNA‐4717‐3p maturation to promote colorectal cancer cell proliferation</title><author>Xu, Qiaolin ; Lu, Xiaoxue ; Li, Jing ; Feng, Yuyang ; Tang, Jie ; Zhang, Tao ; Mao, Yilan ; Lan, Yuanzhi ; Luo, Huaxing ; Zeng, Linghai ; Xiang, Yuanyuan ; Hu, Lv ; Zhang, Yan ; Li, Qian ; Deng, Ling ; He, Xiaoyi ; Tang, Bin ; Mao, Xuhu ; Zeng, Dongzhu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4446-f9c3fc2915de39c8c78b960b6efb3c7837789a306750d2b4a344d5afdb962f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>3' Untranslated regions</topic><topic>Biotechnology</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Epigenetics</topic><topic>Fusobacterium nucleatum</topic><topic>Gene expression</topic><topic>Infections</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>MAP2K4</topic><topic>Maturation</topic><topic>Methylation</topic><topic>Methyltransferase</topic><topic>METTL3</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>miR‐4717‐3p</topic><topic>N6-methyladenosine</topic><topic>Original</topic><topic>Pathogens</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Reagents</topic><topic>Therapeutic targets</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Qiaolin</creatorcontrib><creatorcontrib>Lu, Xiaoxue</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Feng, Yuyang</creatorcontrib><creatorcontrib>Tang, Jie</creatorcontrib><creatorcontrib>Zhang, Tao</creatorcontrib><creatorcontrib>Mao, Yilan</creatorcontrib><creatorcontrib>Lan, Yuanzhi</creatorcontrib><creatorcontrib>Luo, Huaxing</creatorcontrib><creatorcontrib>Zeng, Linghai</creatorcontrib><creatorcontrib>Xiang, Yuanyuan</creatorcontrib><creatorcontrib>Hu, Lv</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Deng, Ling</creatorcontrib><creatorcontrib>He, Xiaoyi</creatorcontrib><creatorcontrib>Tang, Bin</creatorcontrib><creatorcontrib>Mao, Xuhu</creatorcontrib><creatorcontrib>Zeng, Dongzhu</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Qiaolin</au><au>Lu, Xiaoxue</au><au>Li, Jing</au><au>Feng, Yuyang</au><au>Tang, Jie</au><au>Zhang, Tao</au><au>Mao, Yilan</au><au>Lan, Yuanzhi</au><au>Luo, Huaxing</au><au>Zeng, Linghai</au><au>Xiang, Yuanyuan</au><au>Hu, Lv</au><au>Zhang, Yan</au><au>Li, Qian</au><au>Deng, Ling</au><au>He, Xiaoyi</au><au>Tang, Bin</au><au>Mao, Xuhu</au><au>Zeng, Dongzhu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fusobacterium nucleatum induces excess methyltransferase‐like 3‐mediated microRNA‐4717‐3p maturation to promote colorectal cancer cell proliferation</atitle><jtitle>Cancer science</jtitle><date>2022-11</date><risdate>2022</risdate><volume>113</volume><issue>11</issue><spage>3787</spage><epage>3800</epage><pages>3787-3800</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Fusobacterium nucleatum infection plays vital roles in colorectal cancer (CRC) progression. Overexpression of microRNA‐4717‐3p (miR‐4717) was reported to be upregulated in F. nucleatum positive CRC tissues, however, the underlying mechanism is unknown. In this study, we found that miR‐4717 promoted CRC cell proliferation in vitro and growth of CRC in vivo following F. nucleatum infection. MicroRNA‐4717 suppressed the expression of mitogen‐activated protein kinase kinase 4 (MAP2K4), a tumor suppressor, by directly targeting its 3′‐UTR. Furthermore, we confirmed that methyltransferase‐like 3 (METTL3)‐dependent m6A methylation could methylate primary (pri)‐miR‐4717, which further promoted the maturation of pri‐miR‐4717, and METTL3 positively regulated CRC cell proliferation through miR‐4717/MAP2K4 pathways. In conclusion, F. nucleatum‐induced miR‐4717 excessive maturation through METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC.
F. nucleatum‐induced miR‐4717 excessive maturation via METTL3‐dependent m6A modification promotes CRC cell proliferation, which provides a potential therapeutic target and diagnostic biomarker for CRC.</abstract><cop>Tokyo</cop><pub>John Wiley & Sons, Inc</pub><pmid>35984699</pmid><doi>10.1111/cas.15536</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-3540-0728</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1347-9032 |
| ispartof | Cancer science, 2022-11, Vol.113 (11), p.3787-3800 |
| issn | 1347-9032 1349-7006 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9633291 |
| source | DOAJ Directory of Open Access Journals; Access via Wiley Online Library; Wiley Online Library Open Access; PubMed Central |
| subjects | 3' Untranslated regions Biotechnology Cell cycle Cell growth Cell proliferation Colorectal cancer Colorectal carcinoma Epigenetics Fusobacterium nucleatum Gene expression Infections Kinases Laboratory animals MAP2K4 Maturation Methylation Methyltransferase METTL3 MicroRNAs miRNA miR‐4717‐3p N6-methyladenosine Original Pathogens Protein kinase Proteins Reagents Therapeutic targets Tumor suppressor genes Tumors |
| title | Fusobacterium nucleatum induces excess methyltransferase‐like 3‐mediated microRNA‐4717‐3p maturation to promote colorectal cancer cell proliferation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T15%3A13%3A04IST&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=Fusobacterium%20nucleatum%20induces%20excess%20methyltransferase%E2%80%90like%203%E2%80%90mediated%20microRNA%E2%80%904717%E2%80%903p%20maturation%20to%20promote%20colorectal%20cancer%20cell%20proliferation&rft.jtitle=Cancer%20science&rft.au=Xu,%20Qiaolin&rft.date=2022-11&rft.volume=113&rft.issue=11&rft.spage=3787&rft.epage=3800&rft.pages=3787-3800&rft.issn=1347-9032&rft.eissn=1349-7006&rft_id=info:doi/10.1111/cas.15536&rft_dat=%3Cproquest_pubme%3E2704869274%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=2731596827&rft_id=info:pmid/35984699&rfr_iscdi=true |