The exon-junction complex helicase eIF4A3 controls cell fate via coordinated regulation of ribosome biogenesis and translational output
Eukaryotic initiation factor 4A-III (eIF4A3), a core helicase component of the exon junction complex, is essential for splicing, mRNA trafficking, and nonsense-mediated decay processes emerging as targets in cancer therapy. Here, we unravel eIF4A3's tumor-promoting function by demonstrating its...
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| Veröffentlicht in: | Science advances 2021-08, Vol.7 (32), Article 7561 |
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| creator | Kanellis, Dimitris C. Espinoza, Jaime A. Zisi, Asimina Sakkas, Elpidoforos Bartkova, Jirina Katsori, Anna-Maria Bostrom, Johan Dyrskjot, Lars Broholm, Helle Altun, Mikael Elsasser, Simon J. Lindstrom, Mikael S. Bartek, Jiri |
| description | Eukaryotic initiation factor 4A-III (eIF4A3), a core helicase component of the exon junction complex, is essential for splicing, mRNA trafficking, and nonsense-mediated decay processes emerging as targets in cancer therapy. Here, we unravel eIF4A3's tumor-promoting function by demonstrating its role in ribosome biogenesis (RiBi) and p53 (de)regulation. Mechanistically, eIF4A3 resides in nucleoli within the small subunit processome and regulates rRNA processing via R-loop clearance. EIF4A3 depletion induces cell cycle arrest through impaired RiBi checkpoint-mediated p53 induction and reprogrammed translation of cell cycle regulators. Multilevel omics analysis following eIF4A3 depletion pinpoints pathways of cell death regulation and translation of alternative mouse double minute homolog 2 (MDM2) transcript isoforms that control p53. EIF4A3 expression and subnuclear localization among clinical cancer specimens correlate with the RiBi status rendering eIF4A3 an exploitable vulnerability in high-RiBi tumors. We propose a concept of eIF4A3's unexpected role in RiBi, with implications for cancer pathogenesis and treatment. |
| doi_str_mv | 10.1126/sciadv.abf7561 |
| format | Article |
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Here, we unravel eIF4A3's tumor-promoting function by demonstrating its role in ribosome biogenesis (RiBi) and p53 (de)regulation. Mechanistically, eIF4A3 resides in nucleoli within the small subunit processome and regulates rRNA processing via R-loop clearance. EIF4A3 depletion induces cell cycle arrest through impaired RiBi checkpoint-mediated p53 induction and reprogrammed translation of cell cycle regulators. Multilevel omics analysis following eIF4A3 depletion pinpoints pathways of cell death regulation and translation of alternative mouse double minute homolog 2 (MDM2) transcript isoforms that control p53. EIF4A3 expression and subnuclear localization among clinical cancer specimens correlate with the RiBi status rendering eIF4A3 an exploitable vulnerability in high-RiBi tumors. We propose a concept of eIF4A3's unexpected role in RiBi, with implications for cancer pathogenesis and treatment.</description><identifier>ISSN: 2375-2548</identifier><identifier>EISSN: 2375-2548</identifier><identifier>DOI: 10.1126/sciadv.abf7561</identifier><identifier>PMID: 34348895</identifier><language>eng</language><publisher>WASHINGTON: Amer Assoc Advancement Science</publisher><subject>Animals ; Biochemistry ; Cancer ; DEAD-box RNA Helicases - genetics ; DEAD-box RNA Helicases - metabolism ; DNA Helicases - metabolism ; Eukaryotic Initiation Factor-4A - genetics ; Eukaryotic Initiation Factor-4A - metabolism ; Exons - genetics ; Medicin och hälsovetenskap ; Mice ; Multidisciplinary Sciences ; Ribosomes - genetics ; Ribosomes - metabolism ; SciAdv r-articles ; Science & Technology ; Science & Technology - Other Topics ; Tumor Suppressor Protein p53 - genetics</subject><ispartof>Science advances, 2021-08, Vol.7 (32), Article 7561</ispartof><rights>Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).</rights><rights>Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). 2021 The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>33</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000682357400028</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c515t-69e16629f2beebe60eb6fcb726d6061801392bf60a96cd2c127551cc91c4dfb13</citedby><cites>FETCH-LOGICAL-c515t-69e16629f2beebe60eb6fcb726d6061801392bf60a96cd2c127551cc91c4dfb13</cites><orcidid>0000-0002-4253-0275 ; 0000-0002-6937-6124 ; 0000-0001-8690-2010 ; 0000-0002-0731-2715 ; 0000-0001-7061-9851 ; 0000-0001-8724-4849 ; 0000-0003-1148-8497 ; 0000-0003-2013-7525 ; 0000-0001-5252-4023 ; 0000-0002-6029-822X</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/PMC8336962/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8336962/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,553,728,781,785,865,886,2115,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34348895$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-196970$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:147264843$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Kanellis, Dimitris C.</creatorcontrib><creatorcontrib>Espinoza, Jaime A.</creatorcontrib><creatorcontrib>Zisi, Asimina</creatorcontrib><creatorcontrib>Sakkas, Elpidoforos</creatorcontrib><creatorcontrib>Bartkova, Jirina</creatorcontrib><creatorcontrib>Katsori, Anna-Maria</creatorcontrib><creatorcontrib>Bostrom, Johan</creatorcontrib><creatorcontrib>Dyrskjot, Lars</creatorcontrib><creatorcontrib>Broholm, Helle</creatorcontrib><creatorcontrib>Altun, Mikael</creatorcontrib><creatorcontrib>Elsasser, Simon J.</creatorcontrib><creatorcontrib>Lindstrom, Mikael S.</creatorcontrib><creatorcontrib>Bartek, Jiri</creatorcontrib><title>The exon-junction complex helicase eIF4A3 controls cell fate via coordinated regulation of ribosome biogenesis and translational output</title><title>Science advances</title><addtitle>SCI ADV</addtitle><addtitle>Sci Adv</addtitle><description>Eukaryotic initiation factor 4A-III (eIF4A3), a core helicase component of the exon junction complex, is essential for splicing, mRNA trafficking, and nonsense-mediated decay processes emerging as targets in cancer therapy. 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Espinoza, Jaime A. ; Zisi, Asimina ; Sakkas, Elpidoforos ; Bartkova, Jirina ; Katsori, Anna-Maria ; Bostrom, Johan ; Dyrskjot, Lars ; Broholm, Helle ; Altun, Mikael ; Elsasser, Simon J. ; Lindstrom, Mikael S. ; Bartek, Jiri</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-69e16629f2beebe60eb6fcb726d6061801392bf60a96cd2c127551cc91c4dfb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Biochemistry</topic><topic>Cancer</topic><topic>DEAD-box RNA Helicases - genetics</topic><topic>DEAD-box RNA Helicases - metabolism</topic><topic>DNA Helicases - metabolism</topic><topic>Eukaryotic Initiation Factor-4A - genetics</topic><topic>Eukaryotic Initiation Factor-4A - metabolism</topic><topic>Exons - genetics</topic><topic>Medicin och hälsovetenskap</topic><topic>Mice</topic><topic>Multidisciplinary Sciences</topic><topic>Ribosomes - genetics</topic><topic>Ribosomes - metabolism</topic><topic>SciAdv r-articles</topic><topic>Science & Technology</topic><topic>Science & Technology - Other Topics</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kanellis, Dimitris C.</creatorcontrib><creatorcontrib>Espinoza, Jaime A.</creatorcontrib><creatorcontrib>Zisi, Asimina</creatorcontrib><creatorcontrib>Sakkas, Elpidoforos</creatorcontrib><creatorcontrib>Bartkova, Jirina</creatorcontrib><creatorcontrib>Katsori, Anna-Maria</creatorcontrib><creatorcontrib>Bostrom, Johan</creatorcontrib><creatorcontrib>Dyrskjot, Lars</creatorcontrib><creatorcontrib>Broholm, Helle</creatorcontrib><creatorcontrib>Altun, Mikael</creatorcontrib><creatorcontrib>Elsasser, Simon J.</creatorcontrib><creatorcontrib>Lindstrom, Mikael S.</creatorcontrib><creatorcontrib>Bartek, Jiri</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SWEPUB Stockholms universitet full text</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Stockholms universitet</collection><collection>SwePub Articles full text</collection><jtitle>Science advances</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanellis, Dimitris C.</au><au>Espinoza, Jaime A.</au><au>Zisi, Asimina</au><au>Sakkas, Elpidoforos</au><au>Bartkova, Jirina</au><au>Katsori, Anna-Maria</au><au>Bostrom, Johan</au><au>Dyrskjot, Lars</au><au>Broholm, Helle</au><au>Altun, Mikael</au><au>Elsasser, Simon J.</au><au>Lindstrom, Mikael S.</au><au>Bartek, Jiri</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The exon-junction complex helicase eIF4A3 controls cell fate via coordinated regulation of ribosome biogenesis and translational output</atitle><jtitle>Science advances</jtitle><stitle>SCI ADV</stitle><addtitle>Sci Adv</addtitle><date>2021-08-01</date><risdate>2021</risdate><volume>7</volume><issue>32</issue><artnum>7561</artnum><issn>2375-2548</issn><eissn>2375-2548</eissn><abstract>Eukaryotic initiation factor 4A-III (eIF4A3), a core helicase component of the exon junction complex, is essential for splicing, mRNA trafficking, and nonsense-mediated decay processes emerging as targets in cancer therapy. 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| subjects | Animals Biochemistry Cancer DEAD-box RNA Helicases - genetics DEAD-box RNA Helicases - metabolism DNA Helicases - metabolism Eukaryotic Initiation Factor-4A - genetics Eukaryotic Initiation Factor-4A - metabolism Exons - genetics Medicin och hälsovetenskap Mice Multidisciplinary Sciences Ribosomes - genetics Ribosomes - metabolism SciAdv r-articles Science & Technology Science & Technology - Other Topics Tumor Suppressor Protein p53 - genetics |
| title | The exon-junction complex helicase eIF4A3 controls cell fate via coordinated regulation of ribosome biogenesis and translational output |
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