Targeting human 8-oxoguanine DNA glycosylase to mitochondria protects cells from 2-methoxyestradiol-induced-mitochondria-dependent apoptosis

2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17β-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS- hOGG1 ) on HeLa cells exposed to 2-ME. MTS- hOGG1 -expressing cells expos...

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Vydané v:Oncogene Ročník 27; číslo 26; s. 3710 - 3720
Hlavní autori: Chatterjee, A, Chang, X, Nagpal, J K, Chang, S, Upadhyay, S, Califano, J, Trink, B, Sidransky, D
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London Nature Publishing Group UK 12.06.2008
Nature Publishing
Nature Publishing Group
Predmet:
17β-Estradiol
8-Hydroxyguanine
Ageing, cell death
Apoptosis
Apoptosis - drug effects
Biological and medical sciences
Caspase-3
Caspases - physiology
Cell Biology
Cell cycle
Cell Cycle - drug effects
Cell physiology
Cell Survival - drug effects
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cerulenin
Deoxyribonucleic acid
DNA
DNA Damage
DNA glycosylase
DNA Glycosylases - physiology
Estradiol
Estradiol - analogs & derivatives
Estradiol - pharmacology
Estrogens
Fundamental and applied biological sciences. Psychology
Genetics
HeLa Cells
Human Genetics
Humans
Hyperpolarization
Internal Medicine
Medicine
Medicine & Public Health
Membrane potential
Membrane Potential, Mitochondrial - drug effects
Mitochondria
Mitochondria - drug effects
Mitochondrial DNA
Molecular and cellular biology
Oncology
original-article
Physiological aspects
Poly(ADP-ribose)
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerases - metabolism
Ribose
United States
activation
mitochondria
2-methoxyestradiol
Human
Targeting
Enzyme
Fas activation
Activation
Carcinogenesis
Glycosylases
Mitochondria
hOGG1
DNA
Hydrolases
Apoptosis
ISSN:0950-9232, 1476-5594, 1476-5594
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Abstract 2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17β-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS- hOGG1 ) on HeLa cells exposed to 2-ME. MTS- hOGG1 -expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G 2 /M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS- hOGG1 . Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS- hOGG1 . Hence, MTS- hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.
AbstractList 2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17β-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME. MTS-hOGG1-expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G2/M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS-hOGG1. Hence, MTS-hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17beta-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME. MTS-hOGG1-expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G(2)/M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS-hOGG1. Hence, MTS-hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17β-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS- hOGG1 ) on HeLa cells exposed to 2-ME. MTS- hOGG1 -expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G 2 /M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS- hOGG1 . Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS- hOGG1 . Hence, MTS- hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17[beta]- estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME. MTS-hOGG1- expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G sub(2)/M cell cycle arrest compared to vector-only- transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP- ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS- hOGG1. Hence, MTS-hOGG1 plays an important protective role against 2- ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17beta-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME. MTS-hOGG1-expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G(2)/M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS-hOGG1. Hence, MTS-hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17beta-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME. MTS-hOGG1-expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G(2)/M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS-hOGG1. Hence, MTS-hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17beta-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME. MTS-hOGG1-expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G(2)/M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS-hOGG1. Hence, MTS-hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway. [PUBLICATION ABSTRACT]
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17b-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms. We sought to study the effect of mitochondrialy targeted hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME. MTS-hOGG1-expressing cells exposed to 2-ME showed increased cellular survival and had significantly less G sub(2)/M cell cycle arrest compared to vector-only-transfected cells. In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial membrane hyperpolarization, thereby recapitulating the increased expression of MTS-hOGG1. Hence, MTS-hOGG1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis induced through the Fas pathway.Oncogene (2008) 27, 3710-3720; doi:10.1038/onc.2008.3; published online 4 February 2008
Audience Academic
Author Chang, S
Trink, B
Califano, J
Chang, X
Sidransky, D
Nagpal, J K
Upadhyay, S
Chatterjee, A
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ISSN 0950-9232
1476-5594
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IsPeerReviewed true
IsScholarly true
Issue 26
Keywords activation
mitochondria
2-methoxyestradiol
Human
Targeting
Enzyme
Fas activation
Activation
Carcinogenesis
Glycosylases
Mitochondria
hOGG1
DNA
Hydrolases
Apoptosis
Language English
License CC BY 4.0
LinkModel DirectLink
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Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
PMID 18246124
PQID 227368385
PQPubID 36330
PageCount 11
ParticipantIDs proquest_miscellaneous_71667715
proquest_miscellaneous_21333340
proquest_miscellaneous_19744679
proquest_journals_2641391586
proquest_journals_227368385
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pubmed_primary_18246124
pascalfrancis_primary_20435713
crossref_primary_10_1038_onc_2008_3
crossref_citationtrail_10_1038_onc_2008_3
springer_journals_10_1038_onc_2008_3
PublicationCentury 2000
PublicationDate 20080612
PublicationDateYYYYMMDD 2008-06-12
PublicationDate_xml – month: 6
  year: 2008
  text: 20080612
  day: 12
PublicationDecade 2000
PublicationPlace London
PublicationPlace_xml – name: London
– name: Basingstoke
– name: England
– name: New York
PublicationTitle Oncogene
PublicationTitleAbbrev Oncogene
PublicationTitleAlternate Oncogene
PublicationYear 2008
Publisher Nature Publishing Group UK
Nature Publishing
Nature Publishing Group
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing
– name: Nature Publishing Group
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Snippet 2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17β-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms....
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17beta-estradiol, is known to induce mitochondria-mediated apoptosis through several...
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17[beta]- estradiol, is known to induce mitochondria-mediated apoptosis through several...
2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17b-estradiol, is known to induce mitochondria-mediated apoptosis through several mechanisms....
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StartPage 3710
SubjectTerms 17β-Estradiol
8-Hydroxyguanine
Ageing, cell death
Apoptosis
Apoptosis - drug effects
Biological and medical sciences
Caspase-3
Caspases - physiology
Cell Biology
Cell cycle
Cell Cycle - drug effects
Cell physiology
Cell Survival - drug effects
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cerulenin
Deoxyribonucleic acid
DNA
DNA Damage
DNA glycosylase
DNA Glycosylases - physiology
Estradiol
Estradiol - analogs & derivatives
Estradiol - pharmacology
Estrogens
Fundamental and applied biological sciences. Psychology
Genetics
HeLa Cells
Human Genetics
Humans
Hyperpolarization
Internal Medicine
Medicine
Medicine & Public Health
Membrane potential
Membrane Potential, Mitochondrial - drug effects
Mitochondria
Mitochondria - drug effects
Mitochondrial DNA
Molecular and cellular biology
Oncology
original-article
Physiological aspects
Poly(ADP-ribose)
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerases - metabolism
Ribose
Title Targeting human 8-oxoguanine DNA glycosylase to mitochondria protects cells from 2-methoxyestradiol-induced-mitochondria-dependent apoptosis
URI https://link.springer.com/article/10.1038/onc.2008.3
https://www.ncbi.nlm.nih.gov/pubmed/18246124
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Volume 27
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