EMT, cell plasticity and metastasis

Abstract

Carcinoma cells that are induced to suppress their epithelial features and upregulate mesenchymal gene expression programs acquire traits that promote an invasive and metastatic phenotype. This is achieved through the expression of a program termed the epithelial-to-mesenchymal transition (EMT)-a fundamental cell-biological process that plays key roles in embryogenesis and wound healing. Re-activation of the EMT during cancer promotes disease progression and enhances the metastatic phenotype by bestowing upon previously benign carcinoma cell traits such as migration, invasion, resistance to anoikis, chemoresistance and tumour-initiating potential. Herein, we discuss recent insights into the function of the EMT and cancer cell plasticity during cancer progression, with a focus on their role in promoting successful completion of the later stages of the metastatic cascade.

Activation of Notch pathway is linked with epithelial-mesenchymal transition in prostate cancer cells

“…35 Multiple studies have revealed that EMT-type cells acquire enhanced migration and invasion capacity. 36 Therefore, exploring the mechanism of EMT development is required to discover new approaches for the treatment of cancer metastasis.…”

Behind the Scenes: Endo/Exocytosis in the Acquisition of Metastatic Traits

“…These cells are not only the initiators of cancer, by definition, but also represent the subpopulation of cells most likely responsible for metastasis and resistance to therapy (reviewed in ref. 30). Although these findings blur the traditional boundaries between cancer initiation and progression, they offer an additional angle to rationalize the impact of endo/exocytosis in cancer.…”

“…Nevertheless, these results received substantial molecular confirmation from studies showing how EMT can give rise to CSCs, which fuel both tumor growth (due to their self-renewal ability) and metastasis (due to their migratory/invasive ability; ref. 30). An intimate link between migration and tumor growth was proposed recently on the basis of theoretical modeling showing that cellular dispersal and turnover can account for potent selective advantages within a tumor mass (47).…”

A dual phenotype of MDA-MB-468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity

“…In cancer, breakout of cells from solid tumors requires increased motility and reduced cell adhesion. Following their systemic spread via the circulation, the opposite is necessary for the colonization of distal organs, which depends on a ( partial) reversion into less motile cells with regained matrix adhesion (Gunasinghe et al, 2012;Chaffer et al, 2016). However, little is known about the cellular regulation of the underlying adhesion plasticity.…”