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Review

Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial–Mesenchymal Plasticity

1
Department of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 612 65 Brno, Czech Republic
2
International Clinical Research Center, St. Anne’s University Hospital, 656 91 Brno, Czech Republic
3
Department of Experimental Biology, Faculty of Science, Masaryk University, 625 00 Brno, Czech Republic
4
Human Oncology & Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
5
Centre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore 560012, India
*
Author to whom correspondence should be addressed.
Academic Editor: Huey-Jen Lin
Cancers 2021, 13(9), 2188; https://doi.org/10.3390/cancers13092188
Received: 22 April 2021 / Accepted: 29 April 2021 / Published: 2 May 2021
Epithelial–mesenchymal transition (EMT) and its reverse process mesenchymal–epithelial transition (MET) are considered critical events in the cancer progression. These programs are tightly connected with the development of metastasis–the lethal stage of the disease. Both EMT and MET shape the biology of unusually aggressive and heterogeneous triple-negative breast cancer (TNBC). In this review, we summarize the current knowledge of EMT/MET plasticity in the context of TNBC, with a special focus on drivers and mechanisms behind these processes.
Triple-negative breast cancer (TNBC) is a subtype of breast carcinoma known for its unusually aggressive behavior and poor clinical outcome. Besides the lack of molecular targets for therapy and profound intratumoral heterogeneity, the relatively quick overt metastatic spread remains a major obstacle in effective clinical management. The metastatic colonization of distant sites by primary tumor cells is affected by the microenvironment, epigenetic state of particular subclones, and numerous other factors. One of the most prominent processes contributing to the intratumoral heterogeneity is an epithelial–mesenchymal transition (EMT), an evolutionarily conserved developmental program frequently hijacked by tumor cells, strengthening their motile and invasive features. In response to various intrinsic and extrinsic stimuli, malignant cells can revert the EMT state through the mesenchymal–epithelial transition (MET), a process that is believed to be critical for the establishment of macrometastasis at secondary sites. Notably, cancer cells rarely undergo complete EMT and rather exist in a continuum of E/M intermediate states, preserving high levels of plasticity, as demonstrated in primary tumors and, ultimately, in circulating tumor cells, representing a simplified element of the metastatic cascade. In this review, we focus on cellular drivers underlying EMT/MET phenotypic plasticity and its detrimental consequences in the context of TNBC cancer. View Full-Text
Keywords: triple-negative breast cancer; plasticity; epithelial–mesenchymal transition; mesenchymal–epithelial transition; metastasis triple-negative breast cancer; plasticity; epithelial–mesenchymal transition; mesenchymal–epithelial transition; metastasis
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MDPI and ACS Style

Kvokačková, B.; Remšík, J.; Jolly, M.K.; Souček, K. Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial–Mesenchymal Plasticity. Cancers 2021, 13, 2188. https://doi.org/10.3390/cancers13092188

AMA Style

Kvokačková B, Remšík J, Jolly MK, Souček K. Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial–Mesenchymal Plasticity. Cancers. 2021; 13(9):2188. https://doi.org/10.3390/cancers13092188

Chicago/Turabian Style

Kvokačková, Barbora, Ján Remšík, Mohit K. Jolly, and Karel Souček. 2021. "Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial–Mesenchymal Plasticity" Cancers 13, no. 9: 2188. https://doi.org/10.3390/cancers13092188

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