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Targeting androgens via androgen deprivation therapy (ADT) to suppress androgens/androgen receptor (AR) functions remains the standard treatment for prostate cancer. However，most tumors eventually recur in spite of ADT. Here we demonstrate that the prostate epithelial AR may function as asuppresser for prostate cancer metastasis. Results from orthotopically co-inoculated stromal WPMY1 cellswith human epithelial PC3 prostate cancer cells proved that addition of AR in epithelial PC3 cells orknockdown of AR in stromal WPMY1 cells suppressed prostate cancer metastasis. Knockdown of the ARin human CWR22rv1 cells also resulted in increased cell invasion in vitro. Mice lacking the prostateepithelial AR developed larger and more invasive metastatic tumors in lymph nodes and died earlier thanwild-type littermates. In contrast，mice with knockdown of both prostatic epithelia(and stromal ARdeveloped smaller and less invasive metastatic tumors. These data suggest that the epithelial AR is asuppresser and stromal AR is a more dominant stimulator for prostate cancer metastasis. Mechanisticdissection suggested that androgen/AR might modulate many metastasis-related genes via multiplemechanisms. Collectively，these unexpected findings might revolutionize the way we combat prostatecancer，and might allow us to develop new and better therapies，which target the stromal AR only.