| Summary: | Epithelial-to-Mesenchymal transition (EMT) is a developmental programme hijacked by malignant cancer cells to acquire mesenchymal phenotype with invasive ability. Missing in Metastasis (MIM) has been shown as an important protein towards EMT suppression. However, Insulin Receptor Substrate of 53 kDa (IRSp53), a protein with high structural similarity to the N-terminal of MIM has not been characterised for the role in EMT. During epidermal growth factor (EGF)-induced EMT, IRSp53 expression was downregulated which is similar to MIM. To investigate the role of IRSp53 in EMT, an overexpression and a knockdown of IRSp53 expression were performed in the A431 model of EGF-induced EMT. A knockdown of IRSp53 was assessed by changes in molecular markers such as reduction in E-cadherin which led to a loss of cell-cell junctions. An overexpression of IRSp53 inhibited EMT in A431 cells which displayed higher proliferative behaviour. Furthermore, IRSp53 was detected to be localised along cell-cell junctions suggesting an important role in epithelial junction formations together with E-cadherin and actin cytoskeleton. In conclusion, the findings point to upregulation of IRSp53 as a potential strategy for EMT suppression.
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