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Up-regulation of mir-200 and let-7 by natural agents leads to the reversal of epithelial-to-mesenchymal transition in gemcitabine-resistant pancreatic cancer cells
Cancer Research, 08/18/09

Li Y et al. - In a study to compare the expression of miRNAs between gemcitabine-sensitive and gemcitabine-resistant pancreatic cancer (PCa)cells and investigate whether treatment of cells with "natural agents" could affect expression of miRNAs, these results provide experimental evidence that 3,3'-diindolylmethane (DIM) and isoflavone could function as miRNA regulators leading to the reversal of epithelial-to-mesenchymal transition (EMT) phenotype, which is likely to be important for designing novel therapies for PCa.

Methods

Expression of miRNAs was compared between gemcitabine-sensitive and gemcitabine-resistant PCa cells and it was investigated whether treatment of cells with "natural agents" [3,3'-diindolylmethane (DIM) or isoflavone] could affect the expression of miRNAs.

Results

The expression of miR-200b, miR-200c, let-7b, let-7c, let-7d, and let-7e was significantly down-regulated in gemcitabine-resistant cells, which showed EMT characteristics such as elongated fibroblastoid morphology, lower expression of epithelial marker E-cadherin, and higher expression of mesenchymal markers such as vimentin and ZEB1.
Reexpression of miR-200 by transfection studies or treatment of gemcitabine-resistant cells with either DIM or isoflavone resulted in the down-regulation of ZEB1, slug, and vimentin, which was consistent with morphologic reversal of EMT phenotype leading to epithelial morphology.

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