PARP14 regulates cyclin D1 expression to promote cell-cycle progression
Cyclin D1 is an essential regulator of the G1–S cell-cycle transition and is overexpressed in many cancers. Expression of cyclin D1 is under tight cellular regulation that is controlled by many signaling pathways. Here we report that PARP14, a member of the poly(ADP-ribose) polymerase (PARP) family,...
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| Veröffentlicht in: | Oncogene 2021-07, Vol.40 (30), p.4872-4883 |
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| creator | O’Connor, Michael J. Thakar, Tanay Nicolae, Claudia M. Moldovan, George-Lucian |
| description | Cyclin D1 is an essential regulator of the G1–S cell-cycle transition and is overexpressed in many cancers. Expression of cyclin D1 is under tight cellular regulation that is controlled by many signaling pathways. Here we report that PARP14, a member of the poly(ADP-ribose) polymerase (PARP) family, is a regulator of cyclin D1 expression. Depletion of PARP14 leads to decreased cyclin D1 protein levels. In cells with a functional retinoblastoma (RB) protein pathway, this results in G1 cell-cycle arrest and reduced proliferation. Mechanistically, we found that PARP14 controls cyclin D1 mRNA levels. Using luciferase assays, we show that PARP14 specifically regulates cyclin D1 3′UTR mRNA stability. Finally, we also provide evidence that G1 arrest in PARP14-depleted cells is dependent on an intact p53–p21 pathway. Our work uncovers a new role for PARP14 in promoting cell-cycle progression through both cyclin D1 and the p53 pathway. |
| doi_str_mv | 10.1038/s41388-021-01881-8 |
| format | Article |
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Expression of cyclin D1 is under tight cellular regulation that is controlled by many signaling pathways. Here we report that PARP14, a member of the poly(ADP-ribose) polymerase (PARP) family, is a regulator of cyclin D1 expression. Depletion of PARP14 leads to decreased cyclin D1 protein levels. In cells with a functional retinoblastoma (RB) protein pathway, this results in G1 cell-cycle arrest and reduced proliferation. Mechanistically, we found that PARP14 controls cyclin D1 mRNA levels. Using luciferase assays, we show that PARP14 specifically regulates cyclin D1 3′UTR mRNA stability. Finally, we also provide evidence that G1 arrest in PARP14-depleted cells is dependent on an intact p53–p21 pathway. Our work uncovers a new role for PARP14 in promoting cell-cycle progression through both cyclin D1 and the p53 pathway.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-021-01881-8</identifier><identifier>PMID: 34158578</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/106 ; 13/109 ; 13/31 ; 13/89 ; 14 ; 3' Untranslated Regions ; 38 ; 38/77 ; 42 ; 42/41 ; 631/67/395 ; 631/80/641/83 ; Apoptosis ; Breast cancer ; Cancer ; Cell Biology ; Cell cycle ; Cell Cycle - genetics ; Cell growth ; Cell Line ; Cyclin D proteins ; Cyclin D1 ; Cyclin D1 - genetics ; Cyclin D1 - metabolism ; D1 protein ; Development and progression ; DNA repair ; E2F1 Transcription Factor ; G1 Phase Cell Cycle Checkpoints - genetics ; Gene expression ; Gene Expression Regulation ; Gene Knockdown Techniques ; Genes ; Genetic aspects ; Genotype & phenotype ; Health aspects ; Human Genetics ; Humans ; Internal Medicine ; Kinases ; Medicine ; Medicine & Public Health ; mRNA stability ; Mutation ; Oncology ; Oncology, Experimental ; p53 Protein ; Phase transitions ; Phosphorylation ; Poly(ADP-ribose) ; Poly(ADP-ribose) polymerase ; Poly(ADP-ribose) Polymerases - metabolism ; Proteins ; Retina ; Retinoblastoma ; Retinoblastoma protein ; Retinoblastoma Protein - metabolism ; Ribose ; RNA Interference ; RNA Stability ; RNA, Messenger - genetics ; RNA, Small Interfering - genetics ; Transcription factors</subject><ispartof>Oncogene, 2021-07, Vol.40 (30), p.4872-4883</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2021</rights><rights>2021. 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Expression of cyclin D1 is under tight cellular regulation that is controlled by many signaling pathways. Here we report that PARP14, a member of the poly(ADP-ribose) polymerase (PARP) family, is a regulator of cyclin D1 expression. Depletion of PARP14 leads to decreased cyclin D1 protein levels. In cells with a functional retinoblastoma (RB) protein pathway, this results in G1 cell-cycle arrest and reduced proliferation. Mechanistically, we found that PARP14 controls cyclin D1 mRNA levels. Using luciferase assays, we show that PARP14 specifically regulates cyclin D1 3′UTR mRNA stability. Finally, we also provide evidence that G1 arrest in PARP14-depleted cells is dependent on an intact p53–p21 pathway. Our work uncovers a new role for PARP14 in promoting cell-cycle progression through both cyclin D1 and the p53 pathway.</description><subject>13/1</subject><subject>13/106</subject><subject>13/109</subject><subject>13/31</subject><subject>13/89</subject><subject>14</subject><subject>3' Untranslated Regions</subject><subject>38</subject><subject>38/77</subject><subject>42</subject><subject>42/41</subject><subject>631/67/395</subject><subject>631/80/641/83</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Cycle - genetics</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cyclin D proteins</subject><subject>Cyclin D1</subject><subject>Cyclin D1 - genetics</subject><subject>Cyclin D1 - metabolism</subject><subject>D1 protein</subject><subject>Development and progression</subject><subject>DNA repair</subject><subject>E2F1 Transcription Factor</subject><subject>G1 Phase Cell Cycle Checkpoints - 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genetics</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cyclin D proteins</topic><topic>Cyclin D1</topic><topic>Cyclin D1 - genetics</topic><topic>Cyclin D1 - metabolism</topic><topic>D1 protein</topic><topic>Development and progression</topic><topic>DNA repair</topic><topic>E2F1 Transcription Factor</topic><topic>G1 Phase Cell Cycle Checkpoints - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Gene Knockdown Techniques</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genotype & phenotype</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Kinases</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>mRNA stability</topic><topic>Mutation</topic><topic>Oncology</topic><topic>Oncology, Experimental</topic><topic>p53 Protein</topic><topic>Phase transitions</topic><topic>Phosphorylation</topic><topic>Poly(ADP-ribose)</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Proteins</topic><topic>Retina</topic><topic>Retinoblastoma</topic><topic>Retinoblastoma protein</topic><topic>Retinoblastoma Protein - metabolism</topic><topic>Ribose</topic><topic>RNA Interference</topic><topic>RNA Stability</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Small Interfering - genetics</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>O’Connor, Michael J.</creatorcontrib><creatorcontrib>Thakar, Tanay</creatorcontrib><creatorcontrib>Nicolae, Claudia M.</creatorcontrib><creatorcontrib>Moldovan, George-Lucian</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>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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>O’Connor, Michael J.</au><au>Thakar, Tanay</au><au>Nicolae, Claudia M.</au><au>Moldovan, George-Lucian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PARP14 regulates cyclin D1 expression to promote cell-cycle progression</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2021-07-29</date><risdate>2021</risdate><volume>40</volume><issue>30</issue><spage>4872</spage><epage>4883</epage><pages>4872-4883</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Cyclin D1 is an essential regulator of the G1–S cell-cycle transition and is overexpressed in many cancers. Expression of cyclin D1 is under tight cellular regulation that is controlled by many signaling pathways. Here we report that PARP14, a member of the poly(ADP-ribose) polymerase (PARP) family, is a regulator of cyclin D1 expression. Depletion of PARP14 leads to decreased cyclin D1 protein levels. In cells with a functional retinoblastoma (RB) protein pathway, this results in G1 cell-cycle arrest and reduced proliferation. Mechanistically, we found that PARP14 controls cyclin D1 mRNA levels. Using luciferase assays, we show that PARP14 specifically regulates cyclin D1 3′UTR mRNA stability. Finally, we also provide evidence that G1 arrest in PARP14-depleted cells is dependent on an intact p53–p21 pathway. Our work uncovers a new role for PARP14 in promoting cell-cycle progression through both cyclin D1 and the p53 pathway.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>34158578</pmid><doi>10.1038/s41388-021-01881-8</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-3825-149X</orcidid><orcidid>https://orcid.org/0000-0003-4933-5496</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2021-07, Vol.40 (30), p.4872-4883 |
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| subjects | 13/1 13/106 13/109 13/31 13/89 14 3' Untranslated Regions 38 38/77 42 42/41 631/67/395 631/80/641/83 Apoptosis Breast cancer Cancer Cell Biology Cell cycle Cell Cycle - genetics Cell growth Cell Line Cyclin D proteins Cyclin D1 Cyclin D1 - genetics Cyclin D1 - metabolism D1 protein Development and progression DNA repair E2F1 Transcription Factor G1 Phase Cell Cycle Checkpoints - genetics Gene expression Gene Expression Regulation Gene Knockdown Techniques Genes Genetic aspects Genotype & phenotype Health aspects Human Genetics Humans Internal Medicine Kinases Medicine Medicine & Public Health mRNA stability Mutation Oncology Oncology, Experimental p53 Protein Phase transitions Phosphorylation Poly(ADP-ribose) Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerases - metabolism Proteins Retina Retinoblastoma Retinoblastoma protein Retinoblastoma Protein - metabolism Ribose RNA Interference RNA Stability RNA, Messenger - genetics RNA, Small Interfering - genetics Transcription factors |
| title | PARP14 regulates cyclin D1 expression to promote cell-cycle progression |
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