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Biology
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Breast Cancer: Molecular and Cellular Mechanism and Biomarkers
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Breast Cancer: Molecular and Cellular Mechanism and Biomarkers

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

Deadline for manuscript submissions: 30 November 2026 | Viewed by 2170

Special Issue Editors

Dr. Anna Makuch-Kocka

E-Mail Website
Guest Editor
Department of Pharmacology, Faculty of Health Sciences, Medical University of Lublin, 20-400 Lublin, Poland
Interests: breast cancer; apoptosis; multidrug resistance; cancer molecular biology; signal paths
Special Issues, Collections and Topics in MDPI journals
Dr. Przemysław Kołodziej

E-Mail Website
Guest Editor
Department of Biology and Genetics, Faculty of Pharmacy, Medical University of Lublin, 20-093 Lublin, Poland
Interests: transcriptomics; genetic biomarkers; gene expression; medical parasitology; parasitological diagnostics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Breast cancer is one of the most common malignancies in women worldwide. Breast cancer is characterized by great heterogeneity in terms of molecular characteristics, clinical course, prognosis, treatment method, and histopathological features. Currently, developing an effective treatment for this cancer is one of the greatest challenges of modern medicine. In order to increase the percentage of breast cancer cases detected at an early stage of the disease and to develop effective methods of treatment, it is necessary to thoroughly understand the molecular characteristics of this cancer.

The aim of this Special Issue is to gather the latest discoveries related to the molecular biology of breast cancer, from the characterization of the molecular and genetic profile to the latest research results on new potential biomarkers and effective treatment methods for this cancer. We encourage submissions of original or review scientific articles on the broadly understood molecular characterization of breast cancer, including the identification of new biomarkers for early detection, assessment of the stage of advancement or the monitoring of treatment efficacy; genetic characterization of breast cancer; and descriptions of new potential therapeutic targets and factors promoting the development of neoplastic transformation. This Special Issue is also intended for research works taking into account new discoveries in the personalized medicine of breast cancer and understanding the mechanisms of multidrug resistance.

I look forward to receiving your contributions.

Dr. Anna Makuch-Kocka
Dr. Przemysław Kołodziej
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 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. Biology 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 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
  • biomarkers
  • molecular mechanisms
  • multidrug resistance
  • personalized medicine
  • molecular targeted therapy
  • gene expression

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Published Papers (2 papers)

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27 pages, 10362 KB  
Article
Decoding the Clinical and Therapeutic Significance of MEAK7 in Triple-Negative Breast Cancer Through Integrative Bioinformatics
by Durmus Ayan, Meltem Uyaner Kan, Ergul Bayram and Sibel Soylemez
Biology 2026, 15(7), 543; https://doi.org/10.3390/biology15070543 - 28 Mar 2026
Viewed by 770
Abstract
Triple-negative breast cancer (TNBC) represents a clinically challenging breast cancer (BC) subtype, characterized by aggressive behavior, high recurrence risk, and limited therapeutic options. MEAK7 has been identified as an alternative mTORC1 signaling pathway regulator; however, its role in BC and TNBC remains uninvestigated. [...] Read more.
Triple-negative breast cancer (TNBC) represents a clinically challenging breast cancer (BC) subtype, characterized by aggressive behavior, high recurrence risk, and limited therapeutic options. MEAK7 has been identified as an alternative mTORC1 signaling pathway regulator; however, its role in BC and TNBC remains uninvestigated. This study aims to assess MEAK7 expression, prognostic significance, and therapeutic potential. We employed public datasets, including TCGA, bc-GenExMiner v5.2, GEPIA3, DOSurvive platforms, Kaplan–Meier Plotter, UALCAN, TIMER2.0, STRING, ENCORI, HPA, miRDB, TargetScan, and CRISPRdb. MEAK7 expression was significantly elevated in BC tissues versus normal breast tissue. MEAK7 expression was pronounced in TNBC and basal-like subtypes, with hypomethylation of its promoter region in TNBC. Elevated MEAK7 expression correlated with reduced disease-free survival (DFS) in TNBC and basal-like. Multivariate Cox regression identified MEAK7 as a significant prognostic factor for overall survival, independent of age and tumor stage. MEAK7 showed CRISPR-targetable gRNA profiles with high on-target efficiency and minimal off-target effects. Analyses revealed negative correlation with tumor-suppressive RNAs (miR-149-3p, miR-135a-5p, and LINC00993) and positive correlation with aggressive regulators (miR-135b-5p and HIF1A-AS2). This study represents one of the initial comprehensive and multi-platform bioinformatic analyses demonstrating that MEAK7 exhibits elevated expression in breast cancer, particularly within the aggressive TNBC. The findings indicate that MEAK7 may serve as a promising prognostic biomarker in TNBC biology and suggest its viability as a molecular candidate for future investigation in targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Breast Cancer: Molecular and Cellular Mechanism and Biomarkers)
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39 pages, 8540 KB  
Article
Curcumin Enhances Gemcitabine Sensitivity in Breast Cancer Cells Through ROS-Associated Mitochondrial Apoptosis and Transcriptional Reprogramming
by Aşkın Evren Güler, Mehmet Cudi Tuncer and İlhan Özdemir
Biology 2026, 15(5), 448; https://doi.org/10.3390/biology15050448 - 9 Mar 2026
Cited by 1 | Viewed by 691
Abstract
Breast cancer is a leading cause of cancer-related mortality in women, necessitating new treatment strategies. Curcumin (Cur), a natural polyphenol, and gemcitabine (Gem), a standard chemotherapeutic, were investigated for their combined anticancer effects. We hypothesized that Cur sensitizes breast cancer cells to Gem [...] Read more.
Breast cancer is a leading cause of cancer-related mortality in women, necessitating new treatment strategies. Curcumin (Cur), a natural polyphenol, and gemcitabine (Gem), a standard chemotherapeutic, were investigated for their combined anticancer effects. We hypothesized that Cur sensitizes breast cancer cells to Gem via reactive oxygen species (ROS)-mediated apoptosis, and that this effect is associated with selective oxidative vulnerability in malignant cells compared to normal breast epithelial cells. MCF-7 (hormone receptor-positive) and MDA-MB-231 (triple-negative) cells were treated with Cur and Gem alone or in combination. Normal breast epithelial MCF-10A cells were included to evaluate therapeutic selectivity. Cell viability (MTT), apoptosis (Annexin V/PI), oxidative stress (TOS/TAS), intracellular ROS generation (DCFH-DA assay), mitochondrial membrane potential (ΔΨm) (JC-1 staining), caspase activation, synergy (Bliss/HSA/Chou-Talalay), VEGF secretion (ELISA), and transcriptomic changes (RNA-Seq) were assessed. Cur and Gem showed dose-dependent cytotoxicity. Combination treatment demonstrated strong synergistic activity, significantly enhancing apoptosis, oxidative stress, and caspase activation. Direct quantification of intracellular ROS revealed marked ROS accumulation in MCF-7 and MDA-MB-231 cells following combination treatment, whereas MCF-10A cells exhibited only modest oxidative changes. JC-1 analysis demonstrated substantial mitochondrial depolarization in breast cancer cells, which was largely reversible by ROS scavenging and minimal in MCF-10A cells. VEGF secretion was markedly suppressed. Transcriptomic analysis revealed profound alterations in apoptosis, cell cycle, and angiogenesis-related pathways, with more pronounced transcriptional reprogramming observed in the triple-negative subtype. Cur synergistically enhances Gem’s efficacy in breast cancer cells through ROS-mediated apoptosis and anti-angiogenic effects, characterized by cancer-selective ROS amplification and mitochondrial membrane depolarization, supporting its potential as a combination therapy, particularly for triple-negative breast cancer. Full article
(This article belongs to the Special Issue Breast Cancer: Molecular and Cellular Mechanism and Biomarkers)
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