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Zinc finger protein SNAI1 (Snail1) mRNA encodes a key transcription factor that serves as a master regulator of the epithelial-mesenchymal transition (EMT) (UniProt P15172). By repressing the expression of adhesion molecules like E-cadherin, Snail1 enables epithelial cells to acquire a migratory mesenchymal phenotype (PubMed: 10761938). This process is critical during embryonic development and wound healing but is pathologically co-opted in disease (PubMed: 21464214). In the context of oncology, overexpression of Snail1 mRNA is strongly associated with tumor invasion, metastasis, and resistance to conventional therapies (PubMed: 21464214). Snail1 also plays a significant role in the development of organ fibrosis by promoting the activation of myofibroblasts (PubMed: 25605868). Therapeutic strategies targeting Snail1 mRNA, such as antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs), aim to silence its expression to inhibit metastatic progression and sensitize tumors to treatment (PubMed: 30655543). These approaches are currently being explored in preclinical models to address various aggressive cancers and fibrotic conditions.
Targeting of SNAI1 mRNA via RNA interference (siRNA) or antisense oligonucleotides (ASOs) leads to mRNA degradation or translation inhibition, thereby reducing the levels of the Snail1 protein and reversing the epithelial-mesenchymal transition (EMT) phenotype (PubMed: 30655543).
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