Epithelial-mesenchymal plasticity — Engaging stemness in an interplay of phenotypes

Abstract

Cancer is a genetic disease which results in a functional imbalance between tumour-repressive and oncogenic signals. The WHO highlights the burden of this indomitable disease, listing it as the second leading cause of death globally. The major cause of cancer-related death is rarely the effect of the primary tumour itself, but rather, the devastating spread of cancer cells in metastases. Epithelial-mesenchymal plasticity (EMP)—termed as the ability of cells to maintain its plasticity and transit between epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states—plays a fundamental role in cancer metastasis. These cell transitions allow them migrate from the primary tumour and invade the secondary site. EMP is associated with migration, invasion, colonisation, self-renewal and drug resistance. This review briefly elucidates the mechanism of EMP and the association between cancer stem cells (CSCs) and circulating tumour cells (CTCs), biomarkers and signalling pathways involved in EMP as well as drug resistance and therapeutic targeting.