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Regulators of Breast Cancer Metastasis
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Regulators of Breast Cancer Metastasis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Metastasis".

Deadline for manuscript submissions: closed (28 February 2026) | Viewed by 8395

Special Issue Editors

Prof. Dr. Terumi Kohwi-Shigematsu

E-Mail Website
Guest Editor
Biomedical Sciences Graduate Program, University of California, San Francisco, CA, USA
Interests: chromatin organization; genome organizers; DNA structure; transcriptional regulation; epigenetics; cancer metastasis; cancer treatment; cancer diagnosis and prognosis; development
Dr. Saori Furuta

E-Mail Website
Guest Editor
Department of Medicine, Case Western Reserve University, Cleveland, OH, USA
Interests: tumor microenvironment; tumor immunity; immunotherapy; metabolism; microbiome

Special Issue Information

Dear Colleagues,

Targeted therapies for breast cancer have made major advances in recent years. Some therapies known as antibody-drug conjugates can prolong survival of late-stage breast cancer on average of 6-month improvement in prolongation compared to traditional chemotherapy alone. Despite the significant improvement in therapies, metastasis is still the major cause of death from cancer and metastatic breast cancer remains the second leading cause of cancer-associated death of women in the United States. Although breast cancer is known to be a highly heterogeneous disease, it remains true that cancer undergoes progression with time and many acquire the metastatic phenotypes eventually despite the treatment. Therefore, it is important to understand more deeply about the regulatory mechanisms underlying the metastatic phenotypes so that in the future, more effective therapies can be developed to prevent or inhibit cancer progression toward metastasis and recurrence.  In this issue, we aim to address regulation of breast cancer metastasis from broad angles, such as key molecules (e.g. proteins, non-coding RNAs, chemicals), epigenetic and transcriptional regulators, signaling pathways, extracellular environment at primary site (i.e., tumor microenvironment) and distant metastasis site (i.e., metastatic niche), metabolism, immunity, microbiome and aging. Technologies to identify regulators and mechanisms underlying cancer progression are also crucial to develop.  We aim to bring together scientists specialized in different approaches for cancer research in this issue to provide the current perspectives with regards to breast cancer metastasis. We wish to invite review articles and original research studies, focusing on the molecular mechanisms underlying breast cancer progression.

Prof. Dr. Terumi Kohwi-Shigematsu
Dr. Saori Furuta
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tumor progression regulators
  • metastasis
  • tumor microenvironment
  • biomarkers for recurrence
  • transcriptional regulation
  • chromatin structure
  • epigenetics
  • cancer metabolism
  • cancer immunity
  • microbiome

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Published Papers (4 papers)

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Research

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29 pages, 3217 KB  
Article
Chromatin Engagement and Transcriptional Activity of the ZNF217 Exon 4–Skipping Isoform Are Associated with Breast Cancer Aggressiveness and Bone Metastasis
by Pia Fahmé, Lamia Bouazza, Martine Croset, Farah Ramadan, Séverine Croze, Mariapia Riso, Justin Ferraro, Philippe Clézardin, Olivier Peyruchaud, Joël Lachuer, Balázs Győrffy, Robert A. Coleman and Pascale A. Cohen
Cancers 2026, 18(4), 664; https://doi.org/10.3390/cancers18040664 - 18 Feb 2026
Viewed by 386
Abstract
Background: Breast cancer remains a major health issue, with bone metastases negatively impacting patient outcomes. The biochemical and biological functions of the exon 4-splice isoform (ZNF217-ΔE4) of the oncogenic transcription factor ZNF217 have been poorly investigated. Methods/Results: This study, for the first time, [...] Read more.
Background: Breast cancer remains a major health issue, with bone metastases negatively impacting patient outcomes. The biochemical and biological functions of the exon 4-splice isoform (ZNF217-ΔE4) of the oncogenic transcription factor ZNF217 have been poorly investigated. Methods/Results: This study, for the first time, elucidates through advanced live-cell single-molecule tracking microscopy that the C-terminus of ZNF217 influences chromatin engagement and binding stability. ZNF217-ΔE4 retains its ability to be recruited and to promote positive transcriptional activity. CRISPR/Cas9-mediated silencing of the ZNF217 gene in MDA-MB-231 breast cancer cells impairs cell aggressiveness, while reintroduction of the ZNF217-ΔE4 isoform is sufficient to restore increased cell proliferation, migration, invasion, and stemness features. In vivo, ZNF217 ΔE4—although less potent than the wild-type isoform—accelerates the formation of bone marrow micrometastases. A retrospective analysis of primary breast tumors revealed that patients with high ZNF217-ΔE4 mRNA levels had a higher risk of developing bone metastases. Conclusions: Overall, this study identifies ZNF217-ΔE4 as a novel functional isoform that mediates breast cancer cell aggressiveness and bone marrow homing. It also highlights this isoform as a promising biomarker and potential therapeutic target for breast cancers at elevated risk of bone metastasis. Full article
(This article belongs to the Special Issue Regulators of Breast Cancer Metastasis)
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Review

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29 pages, 1855 KB  
Review
The Interplay Between Circadian Clocks and the Tumour Microenvironment in Breast Cancer
by Anna-Marie Finger, Carolin Ector and Valerie M. Weaver
Cancers 2026, 18(6), 925; https://doi.org/10.3390/cancers18060925 - 12 Mar 2026
Viewed by 236
Abstract
Cancer is a heterogeneous systemic disease that is strongly influenced by dynamic interactions with the tumour microenvironment (TME). Despite major advances in understanding spatial and molecular tumour heterogeneity, the temporal dynamics of tumours have received far less attention. Growing evidence has linked circadian [...] Read more.
Cancer is a heterogeneous systemic disease that is strongly influenced by dynamic interactions with the tumour microenvironment (TME). Despite major advances in understanding spatial and molecular tumour heterogeneity, the temporal dynamics of tumours have received far less attention. Growing evidence has linked circadian clocks to cancer risk, progression, and treatment response, including in breast cancer. However, temporal regulation has yet to be recognized as a cancer hallmark, and its interaction with the TME remains poorly understood. This review examines how circadian rhythms organize breast cancer biology through bidirectional interactions with the TME. Circadian clocks coordinate proliferation, DNA damage responses, metabolism, and immune surveillance. Ageing, chronic stress, and obesity, all of which are established breast cancer risk modifiers, disrupt these rhythms and are reciprocally exacerbated by circadian dysfunction, establishing feed-forward loops that accelerate disease. Within the TME, the extracellular matrix (ECM) plays a central role in mediating this bidirectional control. Stiffened fibrotic stroma dampens epithelial clock amplitude, while circadian rhythms in turn shape collagen turnover and ECM remodelling. These dynamics can foster inflammation, stem cell expansion, and metastatic dissemination, including time-of-day-dependent release of circulating breast tumour cells. Systemically, circadian clocks gate immune cell trafficking, creating predictable windows of immunosurveillance and therapeutic vulnerability. By integrating insights from mechanobiology, metabolism, immune regulation, and ageing, we position circadian timing as a unifying layer that connects cell-intrinsic programmes with the evolving breast TME. Understanding these connections opens new opportunities for chronotherapeutic strategies in which treatment timing is aligned with circadian rhythms to improve outcomes. Full article
(This article belongs to the Special Issue Regulators of Breast Cancer Metastasis)
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26 pages, 1511 KB  
Review
Microbiome—Stealth Regulator of Breast Homeostasis and Cancer Metastasis
by Saori Furuta
Cancers 2024, 16(17), 3040; https://doi.org/10.3390/cancers16173040 - 31 Aug 2024
Cited by 7 | Viewed by 3469
Abstract
Cumulative evidence attests to the essential roles of commensal microbes in the physiology of hosts. Although the microbiome has been a major research subject since the time of Luis Pasteur and William Russell over 140 years ago, recent findings that certain intracellular bacteria [...] Read more.
Cumulative evidence attests to the essential roles of commensal microbes in the physiology of hosts. Although the microbiome has been a major research subject since the time of Luis Pasteur and William Russell over 140 years ago, recent findings that certain intracellular bacteria contribute to the pathophysiology of healthy vs. diseased tissues have brought the field of the microbiome to a new era of investigation. Particularly, in the field of breast cancer research, breast-tumor-resident bacteria are now deemed to be essential players in tumor initiation and progression. This is a resurrection of Russel’s bacterial cause of cancer theory, which was in fact abandoned over 100 years ago. This review will introduce some of the recent findings that exemplify the roles of breast-tumor-resident microbes in breast carcinogenesis and metastasis and provide mechanistic explanations for these phenomena. Such information would be able to justify the utility of breast-tumor-resident microbes as biomarkers for disease progression and therapeutic targets. Full article
(This article belongs to the Special Issue Regulators of Breast Cancer Metastasis)
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15 pages, 990 KB  
Review
ELF5: A Molecular Clock for Breast Aging and Cancer Susceptibility
by Masaru Miyano and Mark A. LaBarge
Cancers 2024, 16(2), 431; https://doi.org/10.3390/cancers16020431 - 19 Jan 2024
Cited by 8 | Viewed by 3458
Abstract
Breast cancer is predominantly an age-related disease, with aging serving as the most significant risk factor, compounded by germline mutations in high-risk genes like BRCA1/2. Aging induces architectural changes in breast tissue, particularly affecting luminal epithelial cells by diminishing lineage-specific [...] Read more.
Breast cancer is predominantly an age-related disease, with aging serving as the most significant risk factor, compounded by germline mutations in high-risk genes like BRCA1/2. Aging induces architectural changes in breast tissue, particularly affecting luminal epithelial cells by diminishing lineage-specific molecular profiles and adopting myoepithelial-like characteristics. ELF5 is an important transcription factor for both normal breast and breast cancer development. This review focuses on the role of ELF5 in normal breast development, its altered expression throughout aging, and its implications in cancer. It discusses the lineage-specific expression of ELF5, its regulatory mechanisms, and its potential as a biomarker for breast-specific biological age and cancer risk. Full article
(This article belongs to the Special Issue Regulators of Breast Cancer Metastasis)
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