MET and cancer: These effects are so far known to be mediated, at least in part, via inhibition of mesenchymal-epithelial transition factor (MET) receptor tyrosine kinase and its downstream signaling pathways [25,26], suppression of phosphorylated mechanistic target of rapamycin (mTOR) levels [27], suppression of cyclooxygenase-2 (COX-2) expression [28], and inhibition of signal transducer and activator of transcription 3 (STAT3) [29] in models for various cancer types.