Aims: Breast cancer (BC) is the most frequently occurring cancer in women worldwide. BC patients are often diagnosed at advanced stages which are characterized by low survival rates. Distant metastasis is considered a leading cause of mortalities among BC patients. Epithelial-to-mesenchymal transition (EMT) is a transdifferentiation program that is necessary for cancer cells to acquire metastatic potential. In the last decade, long noncoding RNAs (lncRNAs) proved their significant contribution to different hallmarks of cancer, including EMT and metastasis. The primary aim of our review is to analyze recent studies concerning the molecular mechanisms of lncRNAs implicated in EMT regulation in BC.
Materials and methods: We adopted a comprehensive search on databases of PubMed, Web of Science, and Google Scholar using the following keywords: lncRNAs, EMT, breast cancer, and therapeutic targeting.
Key findings: The different roles of lncRNAs in the mechanisms and signaling pathways governing EMT in BC were summarized. LncRNAs could induce or inhibit EMT through WNT/β-catenin, transforming growth factor-β (TGF-β), Notch, phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), signal transducer and activator of transcription 3 (STAT3), and nuclear factor kappa B (NF-κB) pathways as well as via their interaction with histone modifying complexes and miRNAs.
Significance: LncRNAs are key regulators of EMT and BC metastasis, presenting potential targets for therapeutic interventions. Further research is necessary to investigate the practical application of lncRNAs in clinical therapeutics.
Keywords: Breast cancer; EMT; Invasion; LncRNA; Metastasis; Migration.
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