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Abstract
Melanoma is a highly aggressive malignancy characterized by significant phenotypic plasticity and the co-option of embryonic gene expression programs. Among the critical regulators of this process are the TALE-class homeobox transcription factors MEIS1, MEIS2, and MEIS3. These transcriptional assemblies act as central nodes that integrate hallmark oncogenic signaling pathways, such as the MAPK, PI3K/AKT, and TGF-beta axes, to drive tumor cell survival, proliferation, and invasiveness. The review further explores how MEIS factors influence the epigenetic landscape and phenotypic switching between differentiated and stem-like, dedifferentiated states. By orchestrating these developmental programs, MEIS1-3 proteins fundamentally reinforce the malignant identity of melanoma cells throughout the various stages of cancer progression.
