PARP1 promoter links cell cycle progression with adaptation to oxidative environment

Julita Pietrzak, Corinne M Spickett, Tomasz Płoszajc, László Virág, Agnieszka Robaszkiewicz

Research output: Contribution to journalReview article

Abstract

Although electrophiles are considered as detrimental to cells, accumulating recent evidence indicates that proliferating non-cancerous and particularly cancerous cells utilize these agents for pro-survival and cell cycle promoting signaling. Hence, the redox shift to mild oxidant release must be balanced by multiple defense mechanisms. Our latest findings demonstrate that cell cycle progression, which dictates oxidant level in stress-free conditions, determines PARP1 transcription. Growth modulating factors regulate CDK4/6-RBs-E2Fs axis. In cells arrested in G1 and G0, RB1-E2F1 and RBL2-E2F4 dimers recruit chromatin remodelers such as HDAC1, SWI/SNF and PRC2 to condense chromatin and turn off transcription. Release of retinoblastoma-based repressive complexes from E2F-dependent gene promoters in response to cell transition to S phase enables transcription of PARP1. This enzyme contributes to repair of oxidative DNA damage by supporting several strand break repair pathways and nucleotide or base excision repair pathways, as well as acting as a co-activator of transcription factors such as NRF2 and HIF1a, which control expression of antioxidant enzymes involved in removal of electrophiles and secondary metabolites. Furthermore, PARP1 is indispensible for transcription of the pro-survival kinases MAP2K6, ERK1/2 and AKT1, and for maintaining MAPK activity by suppressing transcription of the MAPK inhibitor, MPK1. In summary, cell cycle controlled PARP1 transcription helps cells to adapt to a pro-oxidant redox shift.
LanguageEnglish
Pages1-5
JournalRedox biology
Volume18
Early online date2 Jun 2018
DOIs
Publication statusE-pub ahead of print - 2 Jun 2018

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Transcription
Cell Cycle
Cells
Repair
Oxidants
DNA Repair
Chromatin
Oxidation-Reduction
Mitogen-Activated Protein Kinase 3
Retinoblastoma
Enzymes
S Phase
DNA Damage
Metabolites
Reactive Oxygen Species
Intercellular Signaling Peptides and Proteins
Transcription Factors
Dimers
Antioxidants
Phosphotransferases

Bibliographical note

Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Funding: R acknowledges grants from Polish National Science Center (DEC-2013/11/D/NZ2/00033) and Ministry of Science and Higher Education (776/STYP/11/2016); CMS acknowledges funding from the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement number 675132; LV acknowledges grants from the National Research, Development and Innovation Office (GINOP-2.3.2-15-2016-00020-TUMORDNS, GINOP-2.3.2-15-2016-00048-STAYALIVE, OTKA K112336).

Cite this

Pietrzak, Julita ; Spickett, Corinne M ; Płoszajc, Tomasz ; Virág, László ; Robaszkiewicz, Agnieszka . / PARP1 promoter links cell cycle progression with adaptation to oxidative environment. In: Redox biology. 2018 ; Vol. 18. pp. 1-5.
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title = "PARP1 promoter links cell cycle progression with adaptation to oxidative environment",
abstract = "Although electrophiles are considered as detrimental to cells, accumulating recent evidence indicates that proliferating non-cancerous and particularly cancerous cells utilize these agents for pro-survival and cell cycle promoting signaling. Hence, the redox shift to mild oxidant release must be balanced by multiple defense mechanisms. Our latest findings demonstrate that cell cycle progression, which dictates oxidant level in stress-free conditions, determines PARP1 transcription. Growth modulating factors regulate CDK4/6-RBs-E2Fs axis. In cells arrested in G1 and G0, RB1-E2F1 and RBL2-E2F4 dimers recruit chromatin remodelers such as HDAC1, SWI/SNF and PRC2 to condense chromatin and turn off transcription. Release of retinoblastoma-based repressive complexes from E2F-dependent gene promoters in response to cell transition to S phase enables transcription of PARP1. This enzyme contributes to repair of oxidative DNA damage by supporting several strand break repair pathways and nucleotide or base excision repair pathways, as well as acting as a co-activator of transcription factors such as NRF2 and HIF1a, which control expression of antioxidant enzymes involved in removal of electrophiles and secondary metabolites. Furthermore, PARP1 is indispensible for transcription of the pro-survival kinases MAP2K6, ERK1/2 and AKT1, and for maintaining MAPK activity by suppressing transcription of the MAPK inhibitor, MPK1. In summary, cell cycle controlled PARP1 transcription helps cells to adapt to a pro-oxidant redox shift.",
author = "Julita Pietrzak and Spickett, {Corinne M} and Tomasz Płoszajc and L{\'a}szl{\'o} Vir{\'a}g and Agnieszka Robaszkiewicz",
note = "Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) Funding: R acknowledges grants from Polish National Science Center (DEC-2013/11/D/NZ2/00033) and Ministry of Science and Higher Education (776/STYP/11/2016); CMS acknowledges funding from the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement number 675132; LV acknowledges grants from the National Research, Development and Innovation Office (GINOP-2.3.2-15-2016-00020-TUMORDNS, GINOP-2.3.2-15-2016-00048-STAYALIVE, OTKA K112336).",
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PARP1 promoter links cell cycle progression with adaptation to oxidative environment. / Pietrzak, Julita; Spickett, Corinne M; Płoszajc, Tomasz; Virág, László ; Robaszkiewicz, Agnieszka .

In: Redox biology, Vol. 18, 02.06.2018, p. 1-5.

Research output: Contribution to journalReview article

TY - JOUR

T1 - PARP1 promoter links cell cycle progression with adaptation to oxidative environment

AU - Pietrzak, Julita

AU - Spickett, Corinne M

AU - Płoszajc, Tomasz

AU - Virág, László

AU - Robaszkiewicz, Agnieszka

N1 - Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) Funding: R acknowledges grants from Polish National Science Center (DEC-2013/11/D/NZ2/00033) and Ministry of Science and Higher Education (776/STYP/11/2016); CMS acknowledges funding from the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement number 675132; LV acknowledges grants from the National Research, Development and Innovation Office (GINOP-2.3.2-15-2016-00020-TUMORDNS, GINOP-2.3.2-15-2016-00048-STAYALIVE, OTKA K112336).

PY - 2018/6/2

Y1 - 2018/6/2

N2 - Although electrophiles are considered as detrimental to cells, accumulating recent evidence indicates that proliferating non-cancerous and particularly cancerous cells utilize these agents for pro-survival and cell cycle promoting signaling. Hence, the redox shift to mild oxidant release must be balanced by multiple defense mechanisms. Our latest findings demonstrate that cell cycle progression, which dictates oxidant level in stress-free conditions, determines PARP1 transcription. Growth modulating factors regulate CDK4/6-RBs-E2Fs axis. In cells arrested in G1 and G0, RB1-E2F1 and RBL2-E2F4 dimers recruit chromatin remodelers such as HDAC1, SWI/SNF and PRC2 to condense chromatin and turn off transcription. Release of retinoblastoma-based repressive complexes from E2F-dependent gene promoters in response to cell transition to S phase enables transcription of PARP1. This enzyme contributes to repair of oxidative DNA damage by supporting several strand break repair pathways and nucleotide or base excision repair pathways, as well as acting as a co-activator of transcription factors such as NRF2 and HIF1a, which control expression of antioxidant enzymes involved in removal of electrophiles and secondary metabolites. Furthermore, PARP1 is indispensible for transcription of the pro-survival kinases MAP2K6, ERK1/2 and AKT1, and for maintaining MAPK activity by suppressing transcription of the MAPK inhibitor, MPK1. In summary, cell cycle controlled PARP1 transcription helps cells to adapt to a pro-oxidant redox shift.

AB - Although electrophiles are considered as detrimental to cells, accumulating recent evidence indicates that proliferating non-cancerous and particularly cancerous cells utilize these agents for pro-survival and cell cycle promoting signaling. Hence, the redox shift to mild oxidant release must be balanced by multiple defense mechanisms. Our latest findings demonstrate that cell cycle progression, which dictates oxidant level in stress-free conditions, determines PARP1 transcription. Growth modulating factors regulate CDK4/6-RBs-E2Fs axis. In cells arrested in G1 and G0, RB1-E2F1 and RBL2-E2F4 dimers recruit chromatin remodelers such as HDAC1, SWI/SNF and PRC2 to condense chromatin and turn off transcription. Release of retinoblastoma-based repressive complexes from E2F-dependent gene promoters in response to cell transition to S phase enables transcription of PARP1. This enzyme contributes to repair of oxidative DNA damage by supporting several strand break repair pathways and nucleotide or base excision repair pathways, as well as acting as a co-activator of transcription factors such as NRF2 and HIF1a, which control expression of antioxidant enzymes involved in removal of electrophiles and secondary metabolites. Furthermore, PARP1 is indispensible for transcription of the pro-survival kinases MAP2K6, ERK1/2 and AKT1, and for maintaining MAPK activity by suppressing transcription of the MAPK inhibitor, MPK1. In summary, cell cycle controlled PARP1 transcription helps cells to adapt to a pro-oxidant redox shift.

UR - https://www.sciencedirect.com/science/article/pii/S2213231718302842

U2 - 10.1016/j.redox.2018.05.017

DO - 10.1016/j.redox.2018.05.017

M3 - Review article

VL - 18

SP - 1

EP - 5

JO - Redox biology

T2 - Redox biology

JF - Redox biology

SN - 2213-2317

ER -