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      Triple-Negative Breast Cancer: Current Understanding and Future Therapeutic Breakthrough Targeting Cancer Stemness

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          Abstract

          Triple-negative breast cancer (TNBC) is cancer that tested as negative for estrogen receptors (ER), progesterone receptors (PR), and excess human epidermal growth factor receptor 2 (HER2) protein which accounts for 15%–20% of all breast cancer cases. TNBC is considered to be a poorer prognosis than other types of breast cancer, mainly because it involves more aggressive phenotypes that are similar to stem cell–like cancer cells (cancer stem cell, CSC). Thus, targeted treatment of TNBC remains a major challenge in clinical practice. This review article surveys the latest evidence concerning the role of genomic alteration in current TNBC treatment responses, current clinical trials and potential targeting sites, CSC and drug resistance, and potential strategies targeting CSCs in TNBC. Furthermore, the role of insulin-like growth factor 1 receptor (IGF-1R) and nicotinic acetylcholine receptors (nAChR) in stemness expression, chemoresistance, and metastasis in TNBC and their relevance to potential treatments are also discussed and highlighted.

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          On the origin of cancer cells.

          O WARBURG (1956)
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            Evolution of the cancer stem cell model.

            Antonija Kreso, John E. Dick (2014)
            Genetic analyses have shaped much of our understanding of cancer. However, it is becoming increasingly clear that cancer cells display features of normal tissue organization, where cancer stem cells (CSCs) can drive tumor growth. Although often considered as mutually exclusive models to describe tumor heterogeneity, we propose that the genetic and CSC models of cancer can be harmonized by considering the role of genetic diversity and nongenetic influences in contributing to tumor heterogeneity. We offer an approach to integrating CSCs and cancer genetic data that will guide the field in interpreting past observations and designing future studies. Copyright © 2014 Elsevier Inc. All rights reserved.
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              IFNalpha activates dormant haematopoietic stem cells in vivo.

              Marieke Essers, Sandra Offner, William E. Blanco-Bose … (2009)
              Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. After injury these cells are induced to proliferate to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNalpha), HSCs efficiently exit G(0) and enter an active cell cycle. HSCs respond to IFNalpha treatment by the increased phosphorylation of STAT1 and PKB/Akt (also known as AKT1), the expression of IFNalpha target genes, and the upregulation of stem cell antigen-1 (Sca-1, also known as LY6A). HSCs lacking the IFNalpha/beta receptor (IFNAR), STAT1 (ref. 3) or Sca-1 (ref. 4) are insensitive to IFNalpha stimulation, demonstrating that STAT1 and Sca-1 mediate IFNalpha-induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-fluoro-uracil, HSCs pre-treated (primed) with IFNalpha and thus induced to proliferate are efficiently eliminated by 5-fluoro-uracil exposure in vivo. Conversely, HSCs chronically activated by IFNalpha are functionally compromised and are rapidly out-competed by non-activatable Ifnar(-/-) cells in competitive repopulation assays. Whereas chronic activation of the IFNalpha pathway in HSCs impairs their function, acute IFNalpha treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNalpha on leukaemic cells, and raise the possibility for new applications of type I interferons to target cancer stem cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancers (Basel)
                Journal ID (iso-abbrev): Cancers (Basel)
                Journal ID (publisher-id): cancers
                Title: Cancers
                Publisher: MDPI
                ISSN (Electronic): 2072-6694
                Publication date (Electronic): 09 September 2019
                Publication date Collection: September 2019
                Volume: 11
                Issue: 9
                Electronic Location Identifier: 1334
                Affiliations
                [1 ]Department of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan (K.-L.L.) (Y.-C.K.)
                [2 ]Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
                [3 ]TMU Research Center for Cell Therapy and Regeneration Medicine, Taipei Medical University, Taipei 11031, Taiwan
                [4 ]TMU Research Center of Cancer Translational Medicine, Taipei Medical University, Taipei 11031, Taiwan
                [5 ]School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan
                [6 ]International PhD Program for Cell Therapy and Regeneration Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
                [7 ]Center for Reproductive Medicine, Taipei Medical University Hospital, Taipei Medical University, Taipei 11031, Taiwan
                [8 ]Comprehensive Cancer Center of Taipei Medical University, Taipei 11031, Taiwan
                [9 ]Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan
                Author notes
                [* ]Correspondence: hoyuansn@ 123456tmu.edu.tw (Y.-S.H.); rita1204@ 123456tmu.edu.tw (Y.-H.H.); Tel.: +886-2-2736-1661 (Ext. 3327) (Y.-S.H.); +886-2-2736-1661 (Ext. 3150) (Y.-H.H.)
                [†]

                The authors contributed equally to this article.

                Author information
                https://orcid.org/0000-0003-1579-3384
                https://orcid.org/0000-0002-9425-7389
                https://orcid.org/0000-0002-3649-6680
                https://orcid.org/0000-0001-6020-9998
                Article
                Publisher ID: cancers-11-01334
                DOI: 10.3390/cancers11091334
                PMC ID: 6769912
                PubMed ID: 31505803
                SO-VID: 09c3a824-2825-4001-95db-c846df56a7b7
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 02 August 2019
                Date accepted : 30 August 2019
                Categories
                Subject: Review

                Keywords: tnbc,recurrence,resistance,cancer stem cell,igf-1r,nachr
                Data availability:
                Keywords: tnbc, recurrence, resistance, cancer stem cell, igf-1r, nachr

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