Breast cancer cells: Focus on the consequences of epithelial-to-mesenchymal transition. (June 2017)

• Record Type: Journal Article
• Authors: Bong, Alice H.L.; Monteith, Gregory R.
• Is Part Of: International journal of biochemistry & cell biology. Volume 87(2017)
• Page Start: 23
• Page End: 26
• Publication Date: 2017-06
• Subjects: ABC ATP-binding cassette -- EGF epidermal growth factor -- EMT epithelial-to-mesenchymal transition -- IGF insulin growth -- MET mesenchymal-to-epithelial transition -- MMP matrix metalloprotease -- PD-L1 programmed death ligand 1 -- PDGFR-A platelet-derived growth factor receptor alpha -- Rac1 ras-related C3 botulinum toxin substrate 1 -- RhoA ras homolog gene family member A -- TGF-β transforming growth factor beta -- TRPM7 transient receptor potential melastatin-like 7; Breast carcinoma -- Mesenchymal -- Plasticity -- Heterogeneity; Biochemistry -- Periodicals; Cytology -- Periodicals; Biochemistry -- Periodicals; Cell Biology -- Periodicals; Biochimie -- Périodiques; Cytologie -- Périodiques; Biochimie; Cytologie; Biochemistry; Cytology; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); Periodicals; 572.05
• DOI: 10.1016/j.biocel.2017.03.014
• Languages: English
• ISSNs: 1357-2725

Abstract

Highlights: Breast tumors are heterogeneous, and cancer cells within a tumor may exhibit epithelial and mesenchymal-like characteristics. Epithelial breast cancer cells can be induced to form mesenchymal-like cells during EMT. The mesenchymal phenotype as a consequence of EMT can be associated with increased resistance to current breast cancer therapies. Abstract: Breast cancers are highly heterogeneous and successful treatment of those subtypes with a high frequency of metastases and resistance to clinically available therapies remains a challenge. An understanding of mechanisms which may contribute to this heterogeneity and generation of more resilient cancer cells is therefore essential. Epithelial-to-mesenchymal transition (EMT) is a dynamic two-way process that occurs during embryonic development and wound healing whereby epithelial cells can gain plasticity and switch to a mesenchymal-like phenotype. EMT has received interest from cancer researchers due to its potential role in processes important in cancer progression and metastasis. Recent evidence has revealed a clear association between EMT and resistance to therapeutics. Targeting of EMT and/or the mesenchymal-like phenotype may be a promising avenue for future therapeutic intervention. This review provides a brief summary of the functional consequences of EMT in breast cancer, with a focus on the mesenchymal-like phenotype.