The role of EMT and MET in cancer dissemination.
Metastatic cancer cells are lethal. Understanding the molecular mechanisms that bolster the conversion from benign to malignant progression is key for treating these heterogeneous and resistant neoplasms. The epithelial-mesenchymal transition (EMT) is a conserved cellular program that alters cell shape, adhesion and movement. The shift to a more mesenchymal-like phenotype can promote tumor cell intravasation of surrounding blood vessels and emigration to a new organ, yet may not be necessary for extravasation or colonization into that environment. Lymphatic dissemination, on the other hand, may not require EMT. This review presents emerging data on the modes by which tumor cells promote EMT/MET via microRNA and prepare the pre-metastatic niche via exosomes.
a Vascular Biology Program, Department of Surgery , Boston Children's Hospital, Harvard Medical School , Boston , MA , USA.
Jacqueline
J
Banyard
a Vascular Biology Program, Department of Surgery , Boston Children's Hospital, Harvard Medical School , Boston , MA , USA.
Diane R
DR
Bielenberg
D000818:Animals; D002454:Cell Differentiation / Q000502:physiology*; D018450:Disease Progression; D058750:Epithelial-Mesenchymal Transition / Q000502:physiology*; D006801:Humans; D009369:Neoplasms / Q000473:pathology*; D014411:Neoplastic Stem Cells / Q000166:cytology*; D010641:Phenotype
Epithelial-mesenchymal transition; exosomes; hematogenous metastasis; lymphatics; lymphogenous metastasis; microRNA