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Mesenchymal–epithelial transition (MET) is a reversible biological process, not a single molecule or receptor. It involves the transformation of motile, spindle-shaped mesenchymal cells into organized arrays of polarized epithelial cells. This transition is crucial during embryonic development for forming tissues and organs—such as during kidney formation where nephrogenic mesenchyme undergoes MET to form renal epithelium[4][7]. The reverse process is called epithelial–mesenchymal transition (EMT) and both processes are essential for normal development, wound healing, tissue regeneration, cancer progression/metastasis reversal, and cellular reprogramming[4][5][6]. MET does not refer to a specific protein or gene but describes coordinated changes in gene expression—upregulation of epithelial genes like E-cadherin and downregulation of mesenchymal genes such as vimentin or N-cadherin[4][7]. While some oncogenic proteins are named similarly—for example "mesenchymal epithelial transition factor" (MET, also known as c-Met), which is an actual receptor tyrosine kinase—the term "mesenchymal–epithelial transition" refers only to the cellular state change/process. Because it is not an individual molecular entity, but rather a complex physiological event involving many signaling pathways and transcription factors (e.g., Snail family), it should not be considered a direct therapeutic target like receptors or enzymes, though its regulation can be therapeutically relevant in cancer biology[4][5]. “A mesenchymal–epithelial transition (MET) is a reversible biological process that involves the transition from motile...mesenchymal cells to planar arrays of polarized cells called epithelia. MET...has been shown to occur in normal development...cancer metastasis and wound healing.”[4] If you intended information about the *receptor tyrosine kinase* commonly abbreviated "MET" ("hepatocyte growth factor receptor"), please clarify your query.
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