Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance

• Published in: Cancer pathogenesis and therapy Vol. 3; no. 2; pp. 120 - 128
• Main Authors: Bangarh, Rashmi, Saini, Reena V., Saini, Adesh K., Singh, Tejveer, Joshi, Hemant, Ramniwas, Seema, Shahwan, Moyad, Tuli, Hardeep Singh
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.03.2025; Elsevier
• Subjects: Cancer drug resistance; Epithelial–mesenchymal transition; Metastasis; Review; Tumor microenvironment; Epithelial–mesenchymal transition; Metastasis; Tumor microenvironment; Cancer drug resistance
• ISSN: 2949-7132; 2097-2563; 2949-7132
• DOI: 10.1016/j.cpt.2024.07.002

Epithelial–mesenchymal transition (EMT) promotes several cancers by increasing tumor cell motility, disrupting epithelial cell phenotypes, apical–basal polarity, and intracellular connections, and enhancing tumor resistance to immunotherapy and chemotherapy. Mesenchymal–epithelial transition (MET), the opposite of EMT, causes tumor metastasis. EMT drives primary tumor cells, whereas MET inhibits them. Importantly, the complex network of EMT includes cell–cell interactions in the tumor microenvironment. Transcription factors, post-translational regulation, cytokine-mediated signaling, and microRNAs control EMT. In this review, we discussed how molecular mechanisms, signaling networks, and epithelial/mesenchymal states affect cancer treatment resistance and the tumor microenvironment. Research on immunotherapy and chemotherapy problems associated with EMT suggests that targeting EMT might be a potential cancer treatment resistance strategy. [Display omitted] •Cancer metastasis is influenced by epithelial–mesenchymal transition (EMT) and mesenchymal–epithelial transition (MET).•Cancer drug resistance is attributed to signaling molecules, epithelial/mesenchymal (E/M) states, and tumor microenvironment.•A possible tactic to combat cancer drug resistance is to target EMT.