Abstract

Abstract. Luminal breast tumors typically have a lower risk of metastasis due to the epithelial nature of the cells. Strong adhesion between epithelial cancer cells lowers their motility, migration rate, and invasive potential. Despite the nature of epithelial breast tumors, they may still undergo metastasis, which is thought to be initiated by epithelial-mesenchymal transition (EMT). EMT is a process through which epithelial cells acquire the phenotype of mesenchymal cells, which have enhanced invasive potential in cancer. MicroRNAs, small regulatory RNAs that inhibit gene expression, play a role in the regulation of EMT. This study demonstrates that microRNA-100 (miR-100) is upregulated in mesenchymal breast cancer cells (MCF-7M) versus epithelial breast cancer cells (MCF-7) via a mammosphere-induced EMT. MiR-100 may play a role in EMT by targeting the insulin like growth factor 1 receptor (IGF1R). Inhibition of miR-100 in MCF-7M cells significantly increased endogenous IGF1R expression. IGF1R has been ...

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