Molecular Mechanism and Therapeutic Opportunities of Breast Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 5 June 2025 | Viewed by 990

Special Issue Editor


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Guest Editor
Department of Nutritional Science and Dietetics, School of Health Sciences, University of the Peloponnese, Antikalamos, 24100 Kalamata, Messinia, Greece
Interests: biochemistry; GPCR signaling; molecular pharmacology; molecular mechanisms of pharmacological action; cell biology; cancer research; drug design

Special Issue Information

Dear Colleagues,

Breast cancer is one of the most frequent cancers worldwide and is characterized by multifactorial etiology and genetic heterogeneity. Molecular mechanisms involved in its pathogenesis include imbalances in cell signaling, metabolism, and stress responses, as well as gene dysfunction. Recent studies have identified new target molecules such as hormone receptors, human epidermal growth factor receptors, and molecular pathways related to cancer cell survival and metastasis. These findings have led to innovative therapeutic strategies, such as targeted antibody therapies, macromolecular and micromolecular inhibitors, and immunotherapies. Personalized medicine based on genomic and tumor profiling offers promising prospects for improving prognosis and reducing side effects. But tackling tumor resistance to treatment and understanding its mechanics is a far greater challenge. As part of the Special Issue, papers could be published that focus on topics such as novel molecular mechanisms involved in the development and progression of breast cancer, targeted therapies, molecular biomarkers, use of genomic analysis for personalized therapy and treatment decisions, immunotherapy, and mechanisms of resistance development, as well as issues related to drug resistance and relapse, and innovative methods for the diagnosis and monitoring of breast cancer.

Dr. Athanasios A. Panagiotopoulos
Guest Editor

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Keywords

  • breast cancer
  • molecular mechanisms
  • targeted therapy
  • genomic profiling
  • hormone receptors
  • tumor microenvironment
  • immunotherapy
  • drug resistance
  • metastasis
  • precision medicine

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Published Papers (1 paper)

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Research

28 pages, 7761 KiB  
Article
Therapeutic Targeting of the Galectin-1/miR-22-3p Axis Regulates Cell Cycle and EMT Depending on the Molecular Subtype of Breast Cancer
by Ju Yeon Kim, Jun Ho Lee, Eun Jung Jung, Young Sim Son, Hee Jin Park, Jae Myung Kim, Taejin Park, Sang-Ho Jeong, Jinkwon Lee, Tae Han Kim, Seon Min Lee and Jeong Doo Heo
Cells 2025, 14(4), 310; https://doi.org/10.3390/cells14040310 - 19 Feb 2025
Viewed by 656
Abstract
Breast cancer is a highly heterogeneous disease; hence, it is crucial to understand its biology and identify new targets for the development of effective treatments. Galectin-1 is known to play an oncogenic role in breast cancer progression. It is known that oncogenic factors [...] Read more.
Breast cancer is a highly heterogeneous disease; hence, it is crucial to understand its biology and identify new targets for the development of effective treatments. Galectin-1 is known to play an oncogenic role in breast cancer progression. It is known that oncogenic factors can influence cancer progression through interactions with miRNAs. The purpose of this study is to identify the clinical significance and biological role of galectin-1 and miR-22-3p in cancer progression according to the molecular subtype of breast cancer. We analyzed the expression of galectin-1 and miR-22-3p using cancer tissues and the correlation with clinical pathological characteristics. In addition, we investigated the regulation of the cell cycle and EMT processes of cancer progression through the galectin-1/miR-22-3p axis using cell lines of different breast cancer subtypes. miR-22-3p negatively regulates galectin-1 expression and the two molecules have opposite patterns of oncogenic and tumor-suppressive functions, respectively; furthermore, these two molecules are associated with metastasis-free survival. Cell experiments showed that miR-22-3p overexpression and galectin-1 knockdown inhibited the proliferation and invasion of breast cancer cells. Galectin-1 regulates different cancer progression pathways depending on the molecular subtype. In hormone receptor-positive breast cancer cells, galectin-1 knockdown mainly inhibited cell cycle-related substances and induced G0/G1 arrest, whereas in triple-negative breast cancer cells, it suppressed molecules related to the epithelial–mesenchymal transition pathway. In conclusion, the miR-22-3p/galectin-1 axis regulates different cancer metastasis mechanisms depending on the specific molecular subtype of breast cancer, and miR-22-3p/galectin-1 axis modulation may be a novel target for molecular subtype-specific personalized treatment. Full article
(This article belongs to the Special Issue Molecular Mechanism and Therapeutic Opportunities of Breast Cancer)
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