Abstract
Plasticity of melanoma and EMT-TF reprogramming
Highlights
Epithelial-mesenchymal transition (EMT) is a reversible embryonic genetic program reactivated in cancer
We addressed the interrelationship between EMTTF network and tumour-initiating pathways in malignant melanoma [4]
Melanoma represents an example of a cancer type solely dependent on the oncogenic pathways initiated by gain-of function mutations in BRAF, NRAS, GRM3 or MEK1/2 with all of them leading to the activation of MEK-ERK module
Summary
Epithelial-mesenchymal transition (EMT) is a reversible embryonic genetic program reactivated in cancer. Melanoma represents an example of a cancer type solely dependent on the oncogenic pathways initiated by gain-of function mutations in BRAF, NRAS, GRM3 or MEK1/2 with all of them leading to the activation of MEK-ERK module. In vitro activation of the MEK-ERK signalling results in the reversion of EMT-TF expression pattern, the downregulation of SNAIL2 and ZEB2 and upregulation of ZEB1/TWIST1.
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