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Molecular Cancer Research
Molecular Cancer Research
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Cancer Genes and Networks

Role of TET1 and 5hmC in an Obesity-Linked Pathway Driving Cancer Stem Cells in Triple-Negative Breast Cancer

Bin Bao, Emily A. Teslow, Cristina Mitrea, Julie L. Boerner, Greg Dyson and Aliccia Bollig-Fischer
Bin Bao
1Barbara Ann Karmanos Cancer Institute and Department of Oncology, Wayne State University School of Medicine, Detroit, Michigan.
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Emily A. Teslow
1Barbara Ann Karmanos Cancer Institute and Department of Oncology, Wayne State University School of Medicine, Detroit, Michigan.
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  • ORCID record for Emily A. Teslow
Cristina Mitrea
2Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
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Julie L. Boerner
1Barbara Ann Karmanos Cancer Institute and Department of Oncology, Wayne State University School of Medicine, Detroit, Michigan.
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Greg Dyson
1Barbara Ann Karmanos Cancer Institute and Department of Oncology, Wayne State University School of Medicine, Detroit, Michigan.
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Aliccia Bollig-Fischer
1Barbara Ann Karmanos Cancer Institute and Department of Oncology, Wayne State University School of Medicine, Detroit, Michigan.
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  • For correspondence: bollig@karmanos.org
DOI: 10.1158/1541-7786.MCR-20-0359 Published December 2020
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Abstract

Triple-negative breast cancer (TNBC) is a subtype of breast cancer that lacks expression of estrogen receptor, progesterone receptor, and the HER2 but is enriched with cancer stem cell–like cells (CSC). CSCs are the fraction of cancer cells recognized as the source of primary malignant tumors that also give rise to metastatic recurrence. 5-Hydroxymethylcytosine (5hmC) is a DNA epigenetic feature derived from 5-methylcytosine by action of tet methylcytosine dioxygenase enzymes (e.g., TET1); and although TET1 and 5hmC are required to maintain embryonic stem cells, the mechanism and role in CSCs remain unknown. Data presented in this report support the conclusion that TET1 and TET1-dependent 5hmC mediate hydrogen peroxide (H2O2)–dependent activation of a novel gene expression cascade driving self-renewal and expansion of CSCs in TNBC. Evidence presented also supports that the H2O2 affecting this pathway arises due to endogenous mechanisms—including downregulation of antioxidant enzyme catalase in TNBC cells—and by exogenous routes, such as systemic inflammation and oxidative stress coupled with obesity, a known risk factor for TNBC incidence and recurrence.

Implications: This study elucidates a pathway dependent on H2O2 and linked to obesity-driven TNBC tumor-initiating CSCs; thus, it provides new understanding that may advance TNBC prevention and treatment strategies.

Footnotes

  • Note: Supplementary data for this article are available at Molecular Cancer Research Online (http://mcr.aacrjournals.org/).

  • Mol Cancer Res 2020;18:1803–14

  • Received April 21, 2020.
  • Revision received August 5, 2020.
  • Accepted September 3, 2020.
  • Published first September 10, 2020.
  • ©2020 American Association for Cancer Research.
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Molecular Cancer Research: 18 (12)
December 2020
Volume 18, Issue 12
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Role of TET1 and 5hmC in an Obesity-Linked Pathway Driving Cancer Stem Cells in Triple-Negative Breast Cancer
Bin Bao, Emily A. Teslow, Cristina Mitrea, Julie L. Boerner, Greg Dyson and Aliccia Bollig-Fischer
Mol Cancer Res December 1 2020 (18) (12) 1803-1814; DOI: 10.1158/1541-7786.MCR-20-0359

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Role of TET1 and 5hmC in an Obesity-Linked Pathway Driving Cancer Stem Cells in Triple-Negative Breast Cancer
Bin Bao, Emily A. Teslow, Cristina Mitrea, Julie L. Boerner, Greg Dyson and Aliccia Bollig-Fischer
Mol Cancer Res December 1 2020 (18) (12) 1803-1814; DOI: 10.1158/1541-7786.MCR-20-0359
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