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Molecular Mechanism and Therapeutic Approaches of Breast Cancer, Metastatic 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: 20 September 2025 | Viewed by 1027

Special Issue Editor


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Guest Editor
1. Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy National Cance Center, Goyang 10408, Republic of Korea
2. Department of Bio-Healthcare, Hwasung Medi-Science University, Hwaseong-si 18274, Republic of Korea
Interests: molecular mechanism; tumor microenvironment; epithelial-to-mesenchymal transition (EMT); post-translational modification (PTM); autophagy; potential therapeutic approaches; preclinical mouse models for cancers; breast cancer; liver cancer; lung cancer; pancreatic cancer; cancer progression and metastasis
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Special Issue Information

Dear Colleagues,

Breast cancers are heterogeneous and have a multistep progression at molecular and morphologic levels during tumor development. Metastatic breast cancer is a cancer that originated in the breast, dispersed into the lymph nodes or several other sites, such as the bone, liver, lung, or brain, and acquired genetic and epigenetic alterations in cancer cells. The molecular mechanisms of the epithelial-to-mesenchymal transition (EMT) are therapeutic targets in metastatic breast cancer. Metastasis is a multistage process that is involved in various epigenetic and post-translational modifications (PTMs) during breast cancer progression and metastasis. The remodeling between the tumor microenvironment and the extracellular matrix (ECM) is also essential for metastasis. Various elements of the breast tumor microenvironment enhance metastatic progression.

This Special Issue, “Molecular Mechanism and Therapeutic Approaches of Breast Cancer, Metastatic Breast Cancer, 3rd Edition”, aims to provide a platform for obtaining new, deeper insights into the molecular mechanisms and potential therapeutic approaches in cancer. Authors are invited to submit original research and topical review articles on these topics.

Dr. Mi Kyung Park
Guest Editor

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Keywords

  • breast cancer
  • metastatic breast cancer
  • epithelial-to-mesenchymal transition (EMT)
  • epigenetic and post-translational modifications (PTM)
  • tumor microenvironment

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Published Papers (1 paper)

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Research

19 pages, 14516 KiB  
Article
MELK as a Mediator of Stemness and Metastasis in Aggressive Subtypes of Breast Cancer
by Breanna McBean, Reine Abou Zeidane, Samuel Lichtman-Mikol, Benjamin Hauk, Johnathan Speers, Savannah Tidmore, Citlally Lopez Flores, Priyanka S. Rana, Courtney Pisano, Meilan Liu, Alyssa Santola, Alberto Montero, Alan P. Boyle and Corey W. Speers
Int. J. Mol. Sci. 2025, 26(5), 2245; https://doi.org/10.3390/ijms26052245 - 3 Mar 2025
Viewed by 759
Abstract
Triple-negative breast cancer (TNBC) is the breast cancer subtype with the poorest prognosis and lacks actionable molecular targets for treatment. Maternal embryonic leucine zipper kinase (MELK) is highly expressed in TNBC and has been implicated in poor clinical outcomes, though its mechanistic role [...] Read more.
Triple-negative breast cancer (TNBC) is the breast cancer subtype with the poorest prognosis and lacks actionable molecular targets for treatment. Maternal embryonic leucine zipper kinase (MELK) is highly expressed in TNBC and has been implicated in poor clinical outcomes, though its mechanistic role in the aggressive biology of TNBC is poorly understood. Here, we demonstrate a role of MELK in TNBC progression and metastasis. Analysis of publicly available datasets revealed that high MELK expression correlates with worse overall survival, recurrence-free survival, and distant metastasis-free survival, and MELK is co-expressed with metastasis-related genes. Functional studies demonstrated that MELK inhibition, using genomic or pharmacologic inhibition, reduces mammosphere formation, migration, and invasion in high-MELK-expressing TNBC cell lines. Conversely, MELK overexpression in low-MELK-expressing cell lines significantly increased invasive capacity in vitro and metastatic potential in vivo, as evidenced by enhanced metastasis to the liver and lungs in a chorioallantoic membrane assay. These findings highlight MELK as a key regulator of TNBC aggressiveness and support its potential as a therapeutic target to mitigate metastasis and improve patient outcomes. Full article
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