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Advances in Biological Breast Cancer Research
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Advances in Biological Breast Cancer Research

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 17021

Special Issue Editors

Prof. Dr. Anna-Mart Engelbrecht

E-Mail Website
Guest Editor
Department of Physiological Sciences, Faculty of Natural Sciences, Stellenbosch University, Stellenbosch 7600, South Africa
Interests: breast cancer; cancer treatment; cancer cells; cell death; animal models
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Joji Mercier

E-Mail Website
Co-Guest Editor
Department of Physiology, University of Pretoria, Pretoria 0007, South Africa
Interests: cancer; cell signaling; cytoskeleton; apoptosis; autophagy; radiation biology; drug discovery; reactive oxygen species
Special Issues, Collections and Topics in MDPI journals
Dr. Iman Van Den Bout

E-Mail Website
Co-Guest Editor
Department of Physiology, Faculty of Health Sciences, University of Pretoria, Pretoria 0007, South Africa
Interests: cellular regulation of cancer cell migration and adhesion; the role of GPCRs in cancer biology and metastasis; development of breast cancer organoid models; breast cancer diagnostics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Breast cancer occurs when carcinogens cause breast epithelial cells to grow uncontrollably. It is one of the most prevalent cancers in the world and the most common type of malignant tumor in women. Fortunately, significant advancements have been made in breast cancer research, improving the success rate of treatment. Using the commonality between breast cancer experimental animal models and human breast cancer in terms of tumor molecular characteristics and biological behavior to study the pathogenesis of various breast cancers and the development of new therapeutic drugs has been particularly helpful. In addition, molecular and cell biology research also contributes to increasing our understanding of breast cancer, leading to more effective diagnosis and treatment options.

In this Special Issue, we aim to collect the latest advances in the study of breast cancer biology, covering mechanisms, diagnosis, regulations, treatment and other related aspects.

Prof. Dr. Anna Mart Engelbrecht
Dr. Joji Mercier
Dr. Iman Van Den Bout
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 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. Biology is an international peer-reviewed open access monthly 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 2700 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

  • breast cancer
  • breast tumor
  • breast cancer cells
  • animal models
  • cell death
  • cancer diagnosis
  • cancer treatment
  • biomarkers
  • cancer microenvironment
  • carcinogens
  • estrogen receptor
  • molecular biology
  • cell biology

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Related Special Issue

Published Papers (10 papers)

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Research

Jump to: Review

16 pages, 2351 KiB  
Article
Investigation of ITGB3 Heterogeneity to Overcome Trastuzumab Resistance in HER2-Positive Breast Cancer
by Asiye Busra Boz Er
Biology 2025, 14(1), 9; https://doi.org/10.3390/biology14010009 - 25 Dec 2024
Viewed by 998
Abstract
HER2-positive breast cancer has an aggressive tumour progression among breast cancers characterized by the overexpression of HER2. Trastuzumab is an FDA-approved drug and has significantly improved outcomes for patients; however, drug resistance remains a major challenge. Tumour heterogeneity, describing genetic, epigenetic, and phenotypic [...] Read more.
HER2-positive breast cancer has an aggressive tumour progression among breast cancers characterized by the overexpression of HER2. Trastuzumab is an FDA-approved drug and has significantly improved outcomes for patients; however, drug resistance remains a major challenge. Tumour heterogeneity, describing genetic, epigenetic, and phenotypic differences within and between tumours, complicates tumour treatment and contributes to drug resistance. Understanding the mechanisms underlying Trastuzumab resistance, such as tumour heterogeneity, is crucial for developing new and effective therapeutic strategies. This study investigates the role of ITGB3 heterogeneity in Trastuzumab resistance, focusing on its impact on TGF-β signalling and migration marker response. It also evaluates the potential of combining Trastuzumab with the integrin β3 inhibitor cilengitide to overcome resistance associated with ITGB3 levels. Trastuzumab-resistant HER2-positive HCC1954 and SKBR3 breast cancer cell lines were generated and analysed for ITGB3 expression heterogeneity. The impact of ITGB3 on TGF-β-responsive genes (WWP1, CARM1, RASGRP1, THBS1, KCTD5, SGCA, EIF3S6, MCAM, FXR2, MTMR3, SOCS3, SLC2A4RG, MMP2, MMP9, and HSP47) and cell migration (Col4a1, fibronectin, ICAM1, Timp2, and vimentin) was analysed using luciferase reporter assays and real-time PCR. The effects of combined treatment with Trastuzumab and cilengitide were also evaluated via wound closure assay. ITGB3 expression varied significantly among resistant clones, correlating with increased expression of TGF-β-responsive genes and enhanced migration markers. Combined treatment with Trastuzumab and cilengitide significantly reduced TGF-β signalling and migration-related gene expression, particularly in high ITGB3-expressing cells. ITGB3 plays a critical role in Trastuzumab resistance through the modulation of TGF-β signalling, migration, and contributing to tumour heterogeneity. Targeting ITGβ3, alone or in combination with cilengitide, offers a promising strategy to resensitize resistant HER2-positive breast cancer cells to Trastuzumab. These findings provide valuable insights into the mechanisms of Trastuzumab resistance and suggest potential therapeutic avenues for improving patient outcomes. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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15 pages, 6900 KiB  
Article
Lower FGFR2 mRNA Expression and Higher Levels of FGFR2 IIIc in HER2-Positive Breast Cancer
by Thérèse Dix-Peek, Caroline Dickens, Juan Valcárcel and Raquel A. B. Duarte
Biology 2024, 13(11), 920; https://doi.org/10.3390/biology13110920 - 13 Nov 2024
Viewed by 1227
Abstract
Fibroblast growth factor receptor 2 (FGFR2) has been associated with breast cancer. We performed in silico analyses to investigate the FGFR2 mRNA expression and splice variants associated with breast cancer subtypes. Online databases, including cBioPortal and TCGA SpliceSeq, were used to examine the [...] Read more.
Fibroblast growth factor receptor 2 (FGFR2) has been associated with breast cancer. We performed in silico analyses to investigate the FGFR2 mRNA expression and splice variants associated with breast cancer subtypes. Online databases, including cBioPortal and TCGA SpliceSeq, were used to examine the association between the FGFR2 expression and splice variants with breast cancer subtypes. A higher FGFR2 mRNA was significantly associated with luminal, oestrogen receptor (ER)-positive breast cancers, and invasive lobular carcinomas, whereas a lower FGFR2 was associated with human epidermal growth factor receptor 2 (HER2)-positive breast cancer and invasive ductal carcinomas. The epithelial alternatively spliced FGFR2 IIIb isoform was significantly enriched in ER+ breast cancer, while the mesenchymal FGFR2 IIIc isoform was significantly prevalent in HER2+ cancer. Increased levels of FGFR2 and IIIb splice isoforms are associated with less aggressive breast cancer phenotypes, while decreased levels of FGFR2 and increased IIIc splice isoform are associated with more aggressive phenotypes. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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20 pages, 4148 KiB  
Article
Genes Related to Motility in an Ionizing Radiation and Estrogen Breast Cancer Model
by Tania Koning and Gloria M. Calaf
Biology 2024, 13(11), 849; https://doi.org/10.3390/biology13110849 - 22 Oct 2024
Viewed by 1566
Abstract
Breast cancer is a major global health concern as it is the primary cause of cancer death for women. Environmental radiation exposure and endogenous factors such as hormones increase breast cancer risk, and its development and spread depend on cell motility and migration. [...] Read more.
Breast cancer is a major global health concern as it is the primary cause of cancer death for women. Environmental radiation exposure and endogenous factors such as hormones increase breast cancer risk, and its development and spread depend on cell motility and migration. The expression of genes associated with cell motility, such as ADAM12, CYR61, FLRT2, SLIT2, VNN1, MYLK, MAP1B, and TUBA1A, was analyzed in an experimental breast cancer model induced by radiation and estrogen. The results showed that TUBA1A, SLIT2, MAP1B, MYLK, and ADAM12 gene expression increased in the irradiated Alpha3 cell line but not in the control or the malignant Tumor2 cell line. Bioinformatic analysis indicated that FLERT2, SLIT2, VNN1, MAP1B, MYLK, and TUBA1A gene expressions were found to be higher in normal tissue than in tumor tissue of breast cancer patients. However, ADAM12 and CYR61 expressions were found to be higher in tumors than in normal tissues, and they had a negative correlation with ESR1 gene expression. Concerning ESR2 gene expression, there was a negative correlation with CYR61, but there was a positive correlation with FLRT2, MYLK, MAP1B, and VNN1. Finally, a decreased survival rate was observed in patients exhibiting high expression levels of TUBA1A and MAP1B. These genes also showed a negative ER status, an important parameter for endocrine therapy. The genes related to motility were affected by ionizing radiation, confirming its role in the initiation process of breast carcinogenesis. In conclusion, the relationship between the patient’s expression of hormone receptors and genes associated with cell motility presents a novel prospect for exploring therapeutic strategies. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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16 pages, 4048 KiB  
Article
Integrative Analysis of ATAC-Seq and RNA-Seq through Machine Learning Identifies 10 Signature Genes for Breast Cancer Intrinsic Subtypes
by Jeong-Woon Park and Je-Keun Rhee
Biology 2024, 13(10), 799; https://doi.org/10.3390/biology13100799 - 7 Oct 2024
Viewed by 3077
Abstract
Breast cancer is a heterogeneous disease composed of various biologically distinct subtypes, each characterized by unique molecular features. Its formation and progression involve a complex, multistep process that includes the accumulation of numerous genetic and epigenetic alterations. Although integrating RNA-seq transcriptome data with [...] Read more.
Breast cancer is a heterogeneous disease composed of various biologically distinct subtypes, each characterized by unique molecular features. Its formation and progression involve a complex, multistep process that includes the accumulation of numerous genetic and epigenetic alterations. Although integrating RNA-seq transcriptome data with ATAC-seq epigenetic information provides a more comprehensive understanding of gene regulation and its impact across different conditions, no classification model has yet been developed for breast cancer intrinsic subtypes based on such integrative analyses. In this study, we employed machine learning algorithms to predict intrinsic subtypes through the integrative analysis of ATAC-seq and RNA-seq data. We identified 10 signature genes (CDH3, ERBB2, TYMS, GREB1, OSR1, MYBL2, FAM83D, ESR1, FOXC1, and NAT1) using recursive feature elimination with cross-validation (RFECV) and a support vector machine (SVM) based on SHAP (SHapley Additive exPlanations) feature importance. Furthermore, we found that these genes were primarily associated with immune responses, hormone signaling, cancer progression, and cellular proliferation. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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17 pages, 2132 KiB  
Article
Inflammation and Tumor Progression: The Differential Impact of SAA in Breast Cancer Models
by Daniel Wilhelm Olivier, Carla Eksteen, Manisha du Plessis, Louis de Jager, Lize Engelbrecht, Nathaniel Wade McGregor, Preetha Shridas, Frederick C. de Beer, Willem J. S. de Villiers, Etheresia Pretorius and Anna-Mart Engelbrecht
Biology 2024, 13(9), 654; https://doi.org/10.3390/biology13090654 - 23 Aug 2024
Viewed by 1607
Abstract
Background: Previous research has shown that the Serum Amyloid A (SAA) protein family is intricately involved in inflammatory signaling and various disease pathologies. We have previously demonstrated that SAA is associated with increased colitis disease severity and the promotion of tumorigenesis. However, the [...] Read more.
Background: Previous research has shown that the Serum Amyloid A (SAA) protein family is intricately involved in inflammatory signaling and various disease pathologies. We have previously demonstrated that SAA is associated with increased colitis disease severity and the promotion of tumorigenesis. However, the specific role of SAA proteins in breast cancer pathology remains unclear. Therefore, we investigated the role of systemic SAA1 and SAA2 (SAA1/2) in a triple-negative breast cancer mouse model. Methods: Syngeneic breast tumors were established in wild-type mice, and mice lacking the SAA1/2 (SAADKO). Subsequently, tumor volume was monitored, species survival determined, the inflammatory profiles of mice assessed with a multiplex assay, and tumor molecular biology and histology characterized with Western blotting and H&E histological staining. Results: WT tumor-bearing mice had increased levels of plasma SAA compared to wild-type control mice, while SAADKO control and tumor-bearing mice presented with lower levels of SAA in their plasma. SAADKO tumor-bearing mice also displayed significantly lower concentrations of systemic inflammatory markers. Tumors from SAADKO mice overall had lower levels of SAA compared to tumors from wild-type mice, decreased apoptosis and inflammasome signaling, and little to no tumor necrosis. Conclusions: We demonstrated that systemic SAA1/2 stimulates the activation of the NLRP3 inflammasome in breast tumors, leading to the production of pro-inflammatory cytokines. This, in turn, promoted apoptosis and tumor necrosis but did not significantly impact tumor growth or histological grading. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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14 pages, 2786 KiB  
Article
Influence of Breast Cancer Extracellular Vesicles on Immune Cell Activation: A Pilot Study
by Jessie Santoro, Barbara Carrese, Maria Sara Peluso, Luigi Coppola, Massimiliano D’Aiuto, Gennaro Mossetti, Marco Salvatore and Giovanni Smaldone
Biology 2023, 12(12), 1531; https://doi.org/10.3390/biology12121531 - 15 Dec 2023
Cited by 5 | Viewed by 2442
Abstract
Breast cancer is the leading cause of cancer-related death in women worldwide. It is well known that breast cancer shows significant alterations in the tumor microenvironment (TME), which is composed of a variety of immune cells, including natural killer (NK) cells, that have [...] Read more.
Breast cancer is the leading cause of cancer-related death in women worldwide. It is well known that breast cancer shows significant alterations in the tumor microenvironment (TME), which is composed of a variety of immune cells, including natural killer (NK) cells, that have a key role in tumor development or anti-tumor responses in breast cancer patients. Luminal B (BT474) and triple-negative breast cancer (HS578T) cell lines were cultured in 2D and 3D model systems. PMBCs from healthy donors were isolated and treated with extracellular vesicles (EVs) from monolayer and spheroids of BT474 and HS578T and analyzed using cytofluorimetric approaches. We observed that EVs can alter the activation and presence of CD335+/CD11b+ NK cells. EVs derived from BT474 and HS578T cells trigger the activation and, simultaneously, a reduction in the percentage of CD335+/CD11b+ NK cells. In addition, EVs derived from BT474 also significantly reduce CD39+ T-regulatory (T-reg) cells. Our preliminary data suggest that using EVs to treat tumors could potentially alter components of the immune system, which causes hyperactivation of specific cell types and can lead to aggressive growth. These data will guide the designing of new personalized diagnostic approaches based on in-depth study of the TME. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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Review

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34 pages, 2242 KiB  
Review
Druggable Molecular Networks in BRCA1/BRCA2-Mutated Breast Cancer
by Francesca Pia Carbone, Pietro Ancona, Stefano Volinia, Anna Terrazzan and Nicoletta Bianchi
Biology 2025, 14(3), 253; https://doi.org/10.3390/biology14030253 - 2 Mar 2025
Viewed by 1294
Abstract
Mutations in the tumor suppressor genes BRCA1 and BRCA2 are associated with the triple-negative breast cancer phenotype, particularly aggressive and hard-to-treat tumors lacking estrogen, progesterone, and human epidermal growth factor receptor 2. This research aimed to understand the metabolic and genetic links behind [...] Read more.
Mutations in the tumor suppressor genes BRCA1 and BRCA2 are associated with the triple-negative breast cancer phenotype, particularly aggressive and hard-to-treat tumors lacking estrogen, progesterone, and human epidermal growth factor receptor 2. This research aimed to understand the metabolic and genetic links behind BRCA1 and BRCA2 mutations and investigate their relationship with effective therapies. Using the Cytoscape software, two networks were generated through a bibliographic analysis of articles retrieved from the PubMed-NCBI database. We identified 98 genes deregulated by BRCA mutations, and 24 were modulated by therapies. In particular, BIRC5, SIRT1, MYC, EZH2, and CSN2 are influenced by BRCA1, while BCL2, BAX, and BRIP1 are influenced by BRCA2 mutation. Moreover, the study evaluated the efficacy of several promising therapies, targeting only BRCA1/BRCA2-mutated cells. In this context, CDDO-Imidazolide was shown to increase ROS levels and induce DNA damage. Similarly, resveratrol decreased the expression of the anti-apoptotic gene BIRC5 while it increased SIRT1 both in vitro and in vivo. Other specific drugs were found to induce apoptosis selectively in BRCA-mutated cells or block cell growth when the mutation occurs, i.e., 3-deazaneplanocin A, genistein or daidzein, and PARP inhibitors. Finally, over-representation analysis on the genes highlights ferroptosis and proteoglycan pathways as potential drug targets for more effective treatments. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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23 pages, 1649 KiB  
Review
Modulation of Wnt/Beta-Catenin Pathway by Major Dietary Phytochemicals Against Breast Cancer Development
by Noah Lieb, Annalisa Tran, Martha Torres and Ajay Bommareddy
Biology 2025, 14(2), 194; https://doi.org/10.3390/biology14020194 - 13 Feb 2025
Viewed by 935
Abstract
Breast cancer is one of the most commonly diagnosed cancers and is the second leading cause of cancer-related deaths among women in the United States. Despite a decrease in mortality associated with breast cancer, there has been a steady increase in its incidence. [...] Read more.
Breast cancer is one of the most commonly diagnosed cancers and is the second leading cause of cancer-related deaths among women in the United States. Despite a decrease in mortality associated with breast cancer, there has been a steady increase in its incidence. Development of the mammary gland is normally regulated by such pathways including Wnt, Hedgehog, estrogen and Notch signaling. However, the deregulation of these pathways gives rise to tumor development, and upregulated Wnt activity along with high levels of beta-catenin is correlated with poor prognosis of breast cancer. In addition, beta-catenin-dependent Wnt signaling is enriched in triple-negative breast cancers and is associated with reduced overall survival in breast cancer patients. Various studies have investigated the ability of naturally occurring plant-based agents to reduce incidence and morbidity of breast cancer by regulating critical cell survival pathways to reverse or inhibit the occurrence of clinical disease. The present review focuses on summarizing the role of commonly consumed dietary phytochemicals and their role in regulating Wnt/β-catenin pathway against the development of breast cancer. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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23 pages, 1210 KiB  
Review
Human Cytomegalovirus Infection and Breast Cancer: A Literature Review of Clinical and Experimental Data
by Rancés Blanco and Juan P. Muñoz
Biology 2025, 14(2), 174; https://doi.org/10.3390/biology14020174 - 8 Feb 2025
Viewed by 1348
Abstract
Breast cancer (BC) remains a significant global health challenge, highlighting the need for continued research into novel risk factors, diagnostic approaches, and personalized treatments. Among emerging risk factors, viral infections have been implicated as potential contributors to breast carcinogenesis and BC progression. Recent [...] Read more.
Breast cancer (BC) remains a significant global health challenge, highlighting the need for continued research into novel risk factors, diagnostic approaches, and personalized treatments. Among emerging risk factors, viral infections have been implicated as potential contributors to breast carcinogenesis and BC progression. Recent evidence suggests that specific oncogenic strains of human cytomegalovirus (HCMV) may have the capacity to transform human mammary epithelial cells. This review assesses clinical data regarding HCMV presence in both tumor and non-tumor breast tissues, examining the role of HCMV oncoproteins in BC development and progression. Current findings indicate a higher prevalence of HCMV infection in breast carcinomas compared to non-tumor tissues, associated with an elevated risk of BC. Additionally, the HCMV-driven breast carcinogenesis model proposed here suggests that HCMV oncoproteins may activate multiple oncogenic pathways, fostering cell proliferation, survival, and tumor development. A deeper understanding of the role of HCMV in BC could enhance risk stratification and support the creation of targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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20 pages, 1045 KiB  
Review
Fetal Mammary Gland Development and Offspring’s Breast Cancer Risk in Adulthood
by Lawrence Mabasa, Anri Kotze, Nonhlakanipho F. Sangweni, Tarryn Willmer, Kwazikwakhe B. Gabuza, Oelfah Patel, Sylvester Ifeanyi Omoruyi, Anathi Burns and Rabia Johnson
Biology 2025, 14(2), 106; https://doi.org/10.3390/biology14020106 - 21 Jan 2025
Viewed by 997
Abstract
While advancements in early detection and improved access to care have significantly enhanced breast cancer survival rates, the disease remains a significant global malignancy, constituting approximately 12.5% of all new cancer cases and claiming nearly 700,000 lives in 2020. As a result, there [...] Read more.
While advancements in early detection and improved access to care have significantly enhanced breast cancer survival rates, the disease remains a significant global malignancy, constituting approximately 12.5% of all new cancer cases and claiming nearly 700,000 lives in 2020. As a result, there is widespread consensus that the most sustainable solution lies in prevention. Indeed, preventive strategies, including lifestyle modifications and research into risk-reducing interventions, offer the potential to address the root causes of noncommunicable diseases such as breast cancer. While conventional wisdom has long attributed established risk factors for breast cancer to age, lifestyle, familial history, and reproductive factors, evidence highlights the maternal environment as a pivotal stage for fetal programming of disease risk, as elucidated in the developmental origins of health and disease (DOHaD) framework. Consequently, a growing body of research has been focused on elucidating epigenomic signatures that influence fetal development while shaping health outcomes and susceptibility to diseases later in life. This review aims to identify fetal mammary developmental genes that have been implicated in breast cancer etiology and the potential interplay of maternal environment in epigenetic programming of breast cancer risk in adulthood. Full article
(This article belongs to the Special Issue Advances in Biological Breast Cancer Research)
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