Mitochondrial SOD2 regulates epithelial–mesenchymal transition and cell populations defined by differential CD44 expression

Epithelial–mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44 low -CD24 high (CD44L) epithelial phenotype to a CD44 hig...

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Published inOncogene Vol. 34; no. 41; pp. 5229 - 5239
Main Authors Kinugasa, H, Whelan, K A, Tanaka, K, Natsuizaka, M, Long, A, Guo, A, Chang, S, Kagawa, S, Srinivasan, S, Guha, M, Yamamoto, K, St Clair, D K, Avadhani, N G, Diehl, J A, Nakagawa, H
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 08.10.2015
Nature Publishing Group
Subjects
13
13/31
38/109
38/89
631/67/327
Antioxidants
Apoptosis
Cancer
CD44 antigen
Cell Biology
Cell death
Cell Line
Cellular biology
Epithelial cells
Epithelial-Mesenchymal Transition
Esophagus
Flow cytometry
Gene expression
Gene Expression Regulation, Enzymologic
Gene regulation
Genetic aspects
Genetic engineering
Health aspects
Homeodomain Proteins - metabolism
Human Genetics
Humans
Hyaluronan Receptors
Immune response
Internal Medicine
Keratinocytes
Medicine
Medicine & Public Health
Mesenchyme
Metastases
Metastasis
Mitochondria
Mitochondria - enzymology
NF-kappa B - metabolism
NF-κB protein
Oncology
original-article
Phenotypes
Properties
Reactive oxygen species
Repressor Proteins - metabolism
Ribonucleic acid
RNA
RNA-mediated interference
Senescence
Superoxide dismutase
Superoxide Dismutase - physiology
Transcription
Zinc Finger E-box Binding Homeobox 2
Online AccessGet full text

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Abstract Epithelial–mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44 low -CD24 high (CD44L) epithelial phenotype to a CD44 high -CD24 −/low (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence; however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT, as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference and flow cytometric approaches, we find that transforming growth factor (TGF)-β stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF-β-mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF-κB and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. These data provide novel mechanistic insights into the dynamic expression of SOD2 during EMT. In addition, we delineate a functional role for SOD2 in EMT via the influence of this antioxidant upon distinct CD44L and CD44H subsets of cancer cells that have been implicated in oral and esophageal tumor biology.
AbstractList Epithelial-mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a [CD44.sup.low]-[CD24.sup.high] (CD44L) epithelial phenotype to a [CD44.sup.high]-[CD24.sup.-/low] (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence;however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently
Epithelial-mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44(low)-CD24(high) (CD44L) epithelial phenotype to a CD44(high)-CD24(-/low) (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence; however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT, as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference and flow cytometric approaches, we find that transforming growth factor (TGF)-β stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF-β-mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF-κB and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. These data provide novel mechanistic insights into the dynamic expression of SOD2 during EMT. In addition, we delineate a functional role for SOD2 in EMT via the influence of this antioxidant upon distinct CD44L and CD44H subsets of cancer cells that have been implicated in oral and esophageal tumor biology.
Epithelial-mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a [CD44.sup.low]-[CD24.sup.high] (CD44L) epithelial phenotype to a [CD44.sup.high]-[CD24.sup.-/low] (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence;however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT, as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference and flow cytometric approaches, we find that transforming growth factor (TGF)-β stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF-β-mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF-κB and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. These data provide novel mechanistic insights into the dynamic expression of SOD2 during EMT. In addition, we delineate a functional role for SOD2 in EMT via the influence of this antioxidant upon distinct CD44L and CD44H subsets of cancer cells that have been implicated in oral and esophageal tumor biology. Oncogene (2015) 34, 5229-5239;doi: 10.1038/onc.2014.449; published online 9 February 2015
Epithelial–mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44low-CD24high (CD44L) epithelial phenotype to a CD44high-CD24−/low (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence; however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT, as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference and flow cytometric approaches, we find that transforming growth factor (TGF)-β stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF-β-mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF-κB and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. These data provide novel mechanistic insights into the dynamic expression of SOD2 during EMT. In addition, we delineate a functional role for SOD2 in EMT via the influence of this antioxidant upon distinct CD44L and CD44H subsets of cancer cells that have been implicated in oral and esophageal tumor biology.
Epithelial–mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44 low -CD24 high (CD44L) epithelial phenotype to a CD44 high -CD24 −/low (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence; however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT, as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference and flow cytometric approaches, we find that transforming growth factor (TGF)-β stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF-β-mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF-κB and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. These data provide novel mechanistic insights into the dynamic expression of SOD2 during EMT. In addition, we delineate a functional role for SOD2 in EMT via the influence of this antioxidant upon distinct CD44L and CD44H subsets of cancer cells that have been implicated in oral and esophageal tumor biology.
Epithelial-mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44 Low -CD24 High (CD44L) epithelial phenotype to a CD44 High -CD24 -/Low (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT while excessive ROS may induce cell death or senescence; however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference (RNAi) and flow cytometric approaches, we find that transforming growth factor (TGF)-β stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF-β-mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF-κB and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. This data provides novel mechanistic insights into the dynamic expression of SOD2 during EMT. Additionally, we delineate a functional role for SOD2 in EMT via the influence of this antioxidant upon distinct CD44L and CD44H subsets of cancer cells that have been implicated in oral and esophageal tumor biology.
Epithelialmesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44low-CD24high (CD44L) epithelial phenotype to a CD44high-CD24/low (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence; however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT, as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference and ow cytometric approaches, we nd that transforming growth factor (TGF)- stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF--mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF-B and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. These data provide novel mechanistic insights into the dynamic expression of SOD2 during EMT.
Epithelial-mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44 super(low)-CD24 super(high) (CD44L) epithelial phenotype to a CD44 super(high)-CD24 super(-/low) (CD44H) mesenchymal phenotype, the latter associated with increased malignant properties of cancer cells. ROS are required for cells undergoing EMT, although excessive ROS may induce cell death or senescence; however, little is known as to how cellular antioxidant capabilities may be regulated during EMT. Mitochondrial superoxide dismutase 2 (SOD2) is frequently overexpressed in oral and esophageal cancers. Here, we investigate mechanisms of SOD2 transcriptional regulation in EMT, as well as the functional role of this antioxidant in EMT. Using well-characterized genetically engineered oral and esophageal human epithelial cell lines coupled with RNA interference and flow cytometric approaches, we find that transforming growth factor (TGF)- beta stimulates EMT, resulting in conversion of CD44L to CD44H cells, the latter of which display SOD2 upregulation. SOD2 induction in transformed keratinocytes was concurrent with suppression of TGF- beta -mediated induction of both ROS and senescence. SOD2 gene expression appeared to be transcriptionally regulated by NF- Kappa B and ZEB2, but not ZEB1. Moreover, SOD2-mediated antioxidant activity may restrict conversion of CD44L cells to CD44H cells at the early stages of EMT. These data provide novel mechanistic insights into the dynamic expression of SOD2 during EMT. In addition, we delineate a functional role for SOD2 in EMT via the influence of this antioxidant upon distinct CD44L and CD44H subsets of cancer cells that have been implicated in oral and esophageal tumor biology.
Audience Academic
Author Kagawa, S
Avadhani, N G
Guo, A
Whelan, K A
Diehl, J A
Tanaka, K
Yamamoto, K
Long, A
Chang, S
Guha, M
St Clair, D K
Nakagawa, H
Kinugasa, H
Natsuizaka, M
Srinivasan, S
AuthorAffiliation 3 Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan
4 Department of Gastroenterology and Hepatology, Hokkaido University, Sapporo, Japan
7 Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina
2 Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania
1 Gastroenterology Division, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
5 Department of Animal Biology, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
6 Graduate Center for Toxicology, University of Kentucky College of Medicine, Lexington, Kentucky
AuthorAffiliation_xml – name: 1 Gastroenterology Division, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
– name: 7 Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina
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– name: 2 Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania
– name: 5 Department of Animal Biology, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
– name: 6 Graduate Center for Toxicology, University of Kentucky College of Medicine, Lexington, Kentucky
– name: 3 Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/25659582$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Macmillan Publishers Limited 2015
COPYRIGHT 2015 Nature Publishing Group
Copyright Nature Publishing Group Oct 8, 2015
Macmillan Publishers Limited 2015.
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SSID ssj0007902
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Snippet Epithelial–mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive...
Epithelial-mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive...
Epithelialmesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen...
SourceID pubmedcentral
proquest
gale
crossref
pubmed
springer
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 5229
SubjectTerms 13
13/31
38/109
38/89
631/67/327
Antioxidants
Apoptosis
Cancer
CD44 antigen
Cell Biology
Cell death
Cell Line
Cellular biology
Epithelial cells
Epithelial-Mesenchymal Transition
Esophagus
Flow cytometry
Gene expression
Gene Expression Regulation, Enzymologic
Gene regulation
Genetic aspects
Genetic engineering
Health aspects
Homeodomain Proteins - metabolism
Human Genetics
Humans
Hyaluronan Receptors
Immune response
Internal Medicine
Keratinocytes
Medicine
Medicine & Public Health
Mesenchyme
Metastases
Metastasis
Mitochondria
Mitochondria - enzymology
NF-kappa B - metabolism
NF-κB protein
Oncology
original-article
Phenotypes
Properties
Reactive oxygen species
Repressor Proteins - metabolism
Ribonucleic acid
RNA
RNA-mediated interference
Senescence
Superoxide dismutase
Superoxide Dismutase - physiology
Transcription
Zinc Finger E-box Binding Homeobox 2
Title Mitochondrial SOD2 regulates epithelial–mesenchymal transition and cell populations defined by differential CD44 expression
URI https://link.springer.com/article/10.1038/onc.2014.449
https://www.ncbi.nlm.nih.gov/pubmed/25659582
https://www.proquest.com/docview/1719973691
https://www.proquest.com/docview/2331620201
https://search.proquest.com/docview/1765954340
https://pubmed.ncbi.nlm.nih.gov/PMC4530096
Volume 34
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