*4.5. Others*

Using microarray analysis, our group had previously showed that several mRNAs and miRNAs become altered in HFD-induced LNCaP xenografts [16,52]. Therefore, complex mechanisms, including candidate pathways mentioned previously, may be considered to contribute to fat-diet induced prostate cancer development and progression. Nara et al. demonstrated that miR-130a was attenuated in HFD-induced prostate cancer progression with MET overexpression in vitro and in vivo and that cytoplasmic MET in prostate cancer tissues was overexpressed in patients with higher body mass index [52]. Kim et al. found that a HFD not only accelerated Src-induced prostate tumorigenesis, but also compromised the inhibitory e ffect of the anticancer drug dasatinib on Src kinase oncogenic potential in vivo [51]. Finally, the association between diet-induced prostate cancer progression and several pathways, including oxidative stress [39], epithelial–mesenchymal transition [40], and basal/luminal di fferentiation [48], have been proposed in previous studies.
