with abilities essential for drug resistance, metastasis, and acquired-tumor stem cell traits. Therefore, inhibition of EMT can be a critical therapeutic strategy for prevention of tumor progression. Forced expression of miR- 200 resulted in abrogation of the capacity of lung cancer cell lines to undergo EMT, invade, and metastasize, and conferred transcriptional features of metastasis-incompetent tumor cells [57]. Restoration of E-cad- herin-mediated cell adhesion is another means by which prevention of EMT in cancer might be possible [58]. Inhibition of EMT by NPI-0052, a protesome inhibitor, via inhibition of nuclear factor-B and Snail has also been demonstrated [59], whereas over-expression of FOXA2 resulted in reduced invasion and suppression of TGF-1-induced EMT [60]. Meanwhile, activation of peroxisome proliferator-activated receptor-g was reported to inhibit TGF--induced EMT in lung cancer cells and prevent metastasis by antagonizing Smad3 function [61]. 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