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Molecular Research and Treatment of Breast Cancer: 3rd Edition
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Molecular Research and Treatment of Breast Cancer: 3rd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (20 May 2025) | Viewed by 10891

Special Issue Editor

Dr. Anna Kawiak

E-Mail Website
Guest Editor
Department of Biotechnology, Intercollegiate Faculty of Biotechnology, University of Gdansk and Medical University of Gdansk, 80-307 Gdansk, Poland
Interests: apoptosis; chemoresistance; cell signaling; natural compounds; anticancer drugs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Breast cancer is one of the most frequently diagnosed malignancies in the female population. Due to its heterogeneity, the molecular mechanisms governing breast cancer development and progression are complex and impact prognosis and treatment efficacy. Advances in the field of molecular research have offered insight into the cellular mechanisms and genetic changes that characterize breast cancer subtypes. This has enabled the identification of key driver genes and aberrations that initiate tumor development and the delineation of signaling pathway alterations underlying breast tumor growth. Furthermore, the characterization of novel cellular targets has significantly contributed to the development of improved therapeutic and diagnostic strategies.

This Special Issue of IJMS will welcome original research and review articles with the aim of providing an overview of advances on the molecular bases of breast cancer. Research within this Issue will focus on the molecular aspects of breast cancer development, progression and invasion. The development and discovery of therapeutic agents, as well as strategies that increase the efficacy of standard therapy, will also be covered. Additionally, research related to therapy resistance and approaches that target tumor escape mechanisms will be included in the scope of this Issue.

More published papers can be found in the closed special issue:

Dr. Anna Kawiak
Guest Editor

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 short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • biomarkers
  • breast cancer
  • cancer stem cells
  • cell signaling
  • circulating tumor cells
  • drug discovery
  • molecular diagnostics
  • molecular profiling
  • targeted therapy
  • therapy resistance

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Related Special Issues

Published Papers (5 papers)

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Research

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24 pages, 4301 KB  
Article
Investigating SMR Peptide Interactions with Breast Cancer-Associated Proteins
by Ming-Bo Huang, Purushottam B. Tiwari, Aykut Üren, Martin N. Shelton, Dara Brena, Jennifer Y. Wu, Mahfuz B. Khan, Michael D. Powell, Jonathan K. Stiles, Erica L. Johnson, Fengxia Yan, Lily Yang and Vincent C. Bond
Int. J. Mol. Sci. 2025, 26(18), 8848; https://doi.org/10.3390/ijms26188848 - 11 Sep 2025
Viewed by 272
Abstract
Breast cancer (BC) is a major cause of cancer-related mortality. Mortalin and Vimentin—two proteins implicated in BC progression and metastasis—have been identified as binding partners of the Secretion Modification Region (SMR) peptide from the HIV Nef protein. These interactions disrupt exosome release and [...] Read more.
Breast cancer (BC) is a major cause of cancer-related mortality. Mortalin and Vimentin—two proteins implicated in BC progression and metastasis—have been identified as binding partners of the Secretion Modification Region (SMR) peptide from the HIV Nef protein. These interactions disrupt exosome release and offer novel therapeutic strategies. This study investigates the binding interactions between the SMR peptide, Mortalin, and Vimentin using surface plasmon resonance (SPR), co-immunoprecipitation (Co-IP), and Western blot assays. We also map the SMR binding sites on Mortalin through scanning peptide mapping and then identify a similar site on the Vimentin protein. Based on these data, we propose that the SMR peptide and its analogs interact with specific amino acid sequences in Mortalin and Vimentin, thereby disrupting cellular processes essential for Epithelial–Mesenchymal Transition (EMT) and tumor progression. SPR analysis revealed that the Nef protein exhibited the highest binding affinity to Vimentin (KD = 0.75 ± 1.1 nM) and Mortalin (KD = 3.16 ± 0.03 nM). The SMRwt peptide also demonstrated direct binding to both proteins with micromolar affinities (KD = 6.63 ± 0.74 µM for Vimentin; KD = 20.73 ± 2.33 µM for Mortalin), though the binding affinity was weaker than the full Nef protein. Co-IP experiments using MDA-MB-231, MCF-7, and BT474 BC cell lines confirmed that SMRwt, but not SMRmut, co-immunoprecipitated with Mortalin. Western blot analysis validated these interactions. Further, Mortalin peptide #56, derived from the substrate-binding domain, did not bind the SMR domain or inhibit Nef function. In contrast, peptides #61 and #62 from the C-terminal domain of Mortalin bound the SMR domain and effectively inhibited Nef activity. Notably, Mortalin peptide #61 inhibited SMRwt binding to both Mortalin and Vimentin, disrupting complex formation on the SPR sensor chip. These findings suggest that specific Mortalin-derived peptides can block SMR interactions, offering a potential therapeutic mechanism. Full article
(This article belongs to the Special Issue Molecular Research and Treatment of Breast Cancer: 3rd Edition)
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17 pages, 2790 KB  
Article
Effective Targeting of Glutamine Synthetase with Amino Acid Analogs as a Novel Therapeutic Approach in Breast Cancer
by Shimaa Abdelsattar, Hiba S. Al-Amodi, Hala F. Kamel, Ahood A. Al-Eidan, Marwa M. Mahfouz, Kareem El khashab, Amany M. Elshamy, Mohamed S. Basiouny, Mohamed A. Khalil, Khaled A. Elawdan, Shorouk Elsaka, Salwa E. Mohamed and Hany Khalil
Int. J. Mol. Sci. 2025, 26(1), 78; https://doi.org/10.3390/ijms26010078 - 25 Dec 2024
Cited by 2 | Viewed by 1997
Abstract
Cancer cells undergo metabolic rewiring to support rapid proliferation and survival in challenging environments. Glutamine is a preferred resource for cancer metabolism, as it provides both carbon and nitrogen for cellular biogenesis. Recent studies suggest the potential anticancer activity of amino acid analogs. [...] Read more.
Cancer cells undergo metabolic rewiring to support rapid proliferation and survival in challenging environments. Glutamine is a preferred resource for cancer metabolism, as it provides both carbon and nitrogen for cellular biogenesis. Recent studies suggest the potential anticancer activity of amino acid analogs. Some of these analogs disrupt cellular nucleotide synthesis, thereby inhibiting the formation of DNA and RNA in cancer cells. In the present study, we investigated the anticancer properties of Acivicin and Azaserine in the breast cancer MCF-7 cell line, comparing their effects to those on the non-tumorigenic MCF-10 epithelial cell line in vitro. Interestingly, at lower concentrations, both Acivicin and Azaserine showed potent inhibition of MCF-7 cell proliferation, as assessed by the MTT assay, without detectable toxicity to normal cells. In contrast, Sorafenib (Nexavar), a commonly used drug for solid tumors, showed harmful effects on normal cells, as indicated by increased lactate dehydrogenase (LDH) production in treated cells. Furthermore, unlike Sorafenib, treatment with Acivicin and Azaserine significantly affected apoptotic signaling in treated cells, indicating the role of both amino acid analogs in activating programmed cell death (PCD), as assessed by the Annexin-V assay, DAPI staining, and the relative expression of tumor suppressor genes PTEN and P53. ELISA analysis of MCF-7 cells revealed that both Acivicin and Azaserine treatments promoted the production of anti-inflammatory cytokines, including IL-4 and IL-10, while significantly reducing the production of tumor necrosis factor alpha (TNF-α). Mechanistically, both Acivicin and Azaserine treatment led to a significant reduction in the expression of glutamine synthetase (GS) at both the RNA and protein levels, resulting in a decrease in intracellular glutamine concentrations over time. Additionally, both treatments showed comparable effects on Raf-1 gene expression and protein phosphorylation when compared with Sorafenib, a Raf-1 inhibitor. Moreover, docking studies confirmed the strong binding affinity between Acivicin, Azaserine, and glutamine synthetase, as evidenced by their docking scores and binding interactions with the enzyme crystal. Collectively, these findings provide evidence for the anticancer activity of the two amino acid analogs Acivicin and Azaserine as antagonists of glutamine synthetase, offering novel insights into potential therapeutic strategies for breast cancer. Full article
(This article belongs to the Special Issue Molecular Research and Treatment of Breast Cancer: 3rd Edition)
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24 pages, 11017 KB  
Article
Altered Phenotypes of Breast Epithelial × Breast Cancer Hybrids after ZEB1 Knock-Out
by Alexander Merckens, Mareike Sieler, Silvia Keil and Thomas Dittmar
Int. J. Mol. Sci. 2023, 24(24), 17310; https://doi.org/10.3390/ijms242417310 - 9 Dec 2023
Cited by 6 | Viewed by 2027
Abstract
ZEB1 plays a pivotal role in epithelial-to-mesenchymal transition (EMT), (cancer) cell stemness and cancer therapy resistance. The M13HS tumor hybrids, which were derived from spontaneous fusion events between the M13SV1-EGFP-Neo breast epithelial cells and HS578T-Hyg breast cancer cells, express ZEB1 and exhibit prospective [...] Read more.
ZEB1 plays a pivotal role in epithelial-to-mesenchymal transition (EMT), (cancer) cell stemness and cancer therapy resistance. The M13HS tumor hybrids, which were derived from spontaneous fusion events between the M13SV1-EGFP-Neo breast epithelial cells and HS578T-Hyg breast cancer cells, express ZEB1 and exhibit prospective cancer stem cell properties. To explore a possible correlation between the ZEB1 and stemness/ EMT-related properties in M13HS tumor hybrids, ZEB1 was knocked-out by CRISPR/Cas9. Colony formation, mammosphere formation, cell migration, invasion assays, flow cytometry and Western blot analyses were performed for the characterization of ZEB1 knock-out cells. The ZEB1 knock-out in M13HS tumor cells was not correlated with the down-regulation of the EMT-related markers N-CADHERIN (CDH2) and VIMENTIN and up-regulation of miR-200c-3p. Nonetheless, both the colony formation and mammosphere formation capacities of the M13HS ZEB1 knock-out cells were markedly reduced. Interestingly, the M13HS-2 ZEB1-KO cells harbored a markedly higher fraction of ALDH1-positive cells. The Transwell/ Boyden chamber migration assay data indicated a reduced migratory activity of the M13HS ZEB1-knock-out tumor hybrids, whereas in scratch/ wound-healing assays only the M13SH-8 ZEB1-knock-out cells possessed a reduced locomotory activity. Similarly, only the M13HS-8 ZEB1-knock-out tumor hybrids showed a reduced invasion capacity. Although the ZEB1 knock-out resulted in only moderate phenotypic changes, our data support the role of ZEB1 in EMT and stemness. Full article
(This article belongs to the Special Issue Molecular Research and Treatment of Breast Cancer: 3rd Edition)
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Review

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24 pages, 2487 KB  
Review
Targeting WEE1 Kinase for Breast Cancer Therapeutics: An Update
by Zhao Zhang, Ritika Harish, Naveed Elahi, Sawanjit Saini, Aamir Telia, Manjit Kundlas, Allexes Koroleva, Israel N. Umoh, Manpreet Lota, Meha Bilkhu, Aladdin Kawaiah, Manogna R. Allala, Armelle Leukeu, Emmanuel Nebuwa, Nadiya Sharifi, Anthony W. Ashton, Xuanmao Jiao and Richard G. Pestell
Int. J. Mol. Sci. 2025, 26(12), 5701; https://doi.org/10.3390/ijms26125701 - 13 Jun 2025
Cited by 1 | Viewed by 2672
Abstract
WEE1 kinase is a crucial cell cycle regulatory protein that controls the timing of mitotic entry. WEE1, via inhibition of Cyclin-dependent Kinase 1 (CDK1) and Cyclin-dependent Kinase 2 (CDK2), governs the G2-M checkpoint by inhibiting entry into mitosis. The state of balance between [...] Read more.
WEE1 kinase is a crucial cell cycle regulatory protein that controls the timing of mitotic entry. WEE1, via inhibition of Cyclin-dependent Kinase 1 (CDK1) and Cyclin-dependent Kinase 2 (CDK2), governs the G2-M checkpoint by inhibiting entry into mitosis. The state of balance between WEE family kinases and CDC25C phosphatases restricts CDK1/CycB activity. The WEE kinase family consists of WEE1, PKMYT1, and WEE2 (WEE1B). WEE1 and PKMYT1 regulate entry into mitosis during cell cycle progression, whereas WEE2 governs cell cycle progression during meiosis. Recent studies have identified WEE1 as a potential therapeutic target in several cancers, including therapy-resistant triple-negative breast cancer. Adavosertib’s clinical promise was challenged by inter-individual variations in response and side effects. Because of these promising preclinical outcomes, other WEE1 kinase inhibitors (Azenosertib, SC0191, IMP7068, PD0407824, PD0166285, WEE1-IN-5, Zedoresertib, WEE1-IN-8, and ATRN-1051) are being developed, with several currently being evaluated in clinical trials or as an adjuvant to chemotherapies. Preclinical studies show WEE1 inhibitors induce MHC class 1 antigens and STING when given as combination therapies, suggesting potential additional therapeutic opportunities. Reliable predictors of clinical responses based on mechanistic insights remain an important unmet need. Herein, we review the role of WEE1 inhibition therapy in breast cancer. Full article
(This article belongs to the Special Issue Molecular Research and Treatment of Breast Cancer: 3rd Edition)
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17 pages, 1957 KB  
Review
Biological Roles and Clinical Applications of Exosomes in Breast Cancer: A Brief Review
by Han Wang, Ruo Wang, Kunwei Shen, Renhong Huang and Zheng Wang
Int. J. Mol. Sci. 2024, 25(9), 4620; https://doi.org/10.3390/ijms25094620 - 24 Apr 2024
Cited by 6 | Viewed by 3033
Abstract
Breast cancer (BC) is a global health risk for women and has a high prevalence rate. The drug resistance, recurrence, and metastasis of BC affect patient prognosis, thus posing a challenge to scientists. Exosomes are extracellular vesicles (EVs) that originate from various cells; [...] Read more.
Breast cancer (BC) is a global health risk for women and has a high prevalence rate. The drug resistance, recurrence, and metastasis of BC affect patient prognosis, thus posing a challenge to scientists. Exosomes are extracellular vesicles (EVs) that originate from various cells; they have a double-layered lipid membrane structure and contain rich biological information. They mediate intercellular communication and have pivotal roles in tumor development, progression, and metastasis and drug resistance. Exosomes are important cell communication mediators in the tumor microenvironment (TME). Exosomes are utilized as diagnostic and prognostic biomarkers for estimating the treatment efficacy of BC and have the potential to function as tools to enable the targeted delivery of antitumor drugs. This review introduces recent progress in research on how exosomes influence tumor development and the TME. We also present the research progress on the application of exosomes as prognostic and diagnostic biomarkers and drug delivery tools. Full article
(This article belongs to the Special Issue Molecular Research and Treatment of Breast Cancer: 3rd Edition)
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