Stromal-Modulated Epithelial-to-Mesenchymal Transition in Cancer Cells

The ability of cancer cells to detach from the primary site and metastasize is the main cause of cancer- related death among all cancer types. Epithelial-to-mesenchymal transition (EMT) is the first event of the metastatic cascade, resulting in the loss of cell-cell adhesion and the acquisition of motile and stem-like phenotypes. A critical modulator of EMT in cancer cells is the stromal tumor microenvironment (TME), which can promote the acquisition of a mesenchymal phenotype through direct interaction with cancer cells or changes to the broader microenvironment. In this review, we will explore the role of stromal cells in modulating cancer cell EMT, with particular emphasis on the function of mesenchymal stromal/stem cells (MSCs) through the activation of EMT-inducing pathways, extra cellular matrix (ECM) remodeling, immune cell alteration, and metabolic rewiring.

Automated summary

The ability of cancer cells to detach from the primary site and metastasize is the main cause of cancer-related death. The first event in the metastatic cascade is epithelial-to-mesenchymal transition (EMT), which leads to the loss of cell-cell adhesion and the acquisition of motile and stem-like phenotypes. The tumor microenvironment (TME) plays a critical role in modulating EMT in cancer cells, promoting the acquisition of a mesenchymal phenotype through interaction or changes with cancer cells.