Abstract
High levels of chemokine (C-C motif) ligand 2 (CCL2) promote the metastatic dissemination of prostate cancer by recruiting macrophages to neoplastic lesions. We have recently discovered that inhibiting the androgen receptor (AR) in prostate cancer cells or tumor-infiltrating macrophages results in the upregulation CCL2 and promotes disease progression by activating signal transducer and activator of transcription 3 (STAT3) and by favoring the epithelial-to-mesenchymal transition. Our results indicate that the sole inhibition of AR as a therapeutic intervention against prostate cancer is intrinsically destined to failed.