Androgen deprivation therapy (ADT) is the standard treatment for prostate cancer (PCa), but it is often followed by the development of resistance, leading to the progression of castration-resistant prostate cancer. A key factor influencing treatment response, disease progression, and prognosis is the tumor immune microenvironment. Notably, the accumulation of myeloid-derived suppressor cells (MDSCs) within the tumor creates an immunosuppressive milieu, contributing to treatment failure. Interactions between MDSCs and tumor cells in PCa have been shown to drive castration resistance and facilitate tumor progression. Targeting this immunosuppressive microenvironment holds significant promise for improving therapeutic outcomes. Strategies to target MDSCs include modulating their immunosuppressive activity, promoting their maturation, or inducing their apoptosis. While monotherapy with immunotherapy has shown limited survival benefits in PCa, combining MDSC-targeted therapies with immunotherapy may significantly enhance treatment efficacy and patient outcomes. This review aims to examine the role of MDSCs in therapy resistance and explore potential strategies for targeting them in PCa.
Liu et al. (Wed,) studied this question.