SNAI1

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SNAI1


SNAI1 (Snail Family Transcriptional Repressor 1) is a protein that in humans is encoded by the SNAI1 gene. It plays a crucial role in the process of Epithelial-mesenchymal transition (EMT), which is vital for embryonic development and has been implicated in the progression of various types of cancer. SNAI1 functions as a transcriptional repressor by binding to E-box motifs on target genes, leading to the downregulation of epithelial markers such as E-cadherin, and the upregulation of mesenchymal markers, facilitating the transition from an epithelial to a mesenchymal phenotype.

Function[edit | edit source]

SNAI1 is involved in numerous biological processes, including development, cell migration, invasion, and tumor progression. By repressing E-cadherin, SNAI1 promotes the loss of cell-cell adhesion and increases cell motility, which is essential for embryonic development and wound healing. However, this same mechanism contributes to the invasive and metastatic properties of cancer cells.

Clinical Significance[edit | edit source]

The aberrant expression of SNAI1 has been linked to the progression and metastasis of several types of cancers, including breast cancer, colorectal cancer, and hepatocellular carcinoma. Its role in EMT and cancer progression makes it a potential target for therapeutic intervention.

Regulation[edit | edit source]

The expression and activity of SNAI1 are regulated at multiple levels, including transcriptional, post-transcriptional, and post-translational modifications. Factors such as growth factors, cytokines, and hypoxia can induce the expression of SNAI1. Additionally, post-translational modifications such as phosphorylation and ubiquitination affect its stability and function.

Research[edit | edit source]

Ongoing research is focused on understanding the detailed mechanisms by which SNAI1 regulates EMT and its implications in cancer and other diseases. Studies are also exploring potential strategies to target SNAI1 for cancer therapy.


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Contributors: Prab R. Tumpati, MD