PIM Kinase Inhibition Reprograms Macrophages to Boost Immunotherapy in Prostate Cancer

نویسندگان

1 Department of Biology, SR.C., Islamic Azad University, Tehran, Iran

doi
10.22034/tru.2025.553638.1291
چکیده

Despite the transformative success of immunotherapy in various cancers, its efficacy in prostate cancer remains limited due to the tumor’s immunosuppressive microenvironment and poor T-cell infiltration. This editorial examines the multifaceted roles of PIM kinases, specifically PIM1, PIM2, and PIM3, in driving prostate cancer progression, immune evasion, and therapeutic resistance. PIM kinases promote oncogenic signaling, suppress apoptosis, and upregulate immunosuppressive molecules such as PD-L1 and PD-L2, thereby attenuating anti-tumor immune responses. Their influence extends to the tumor microenvironment, where they modulate tumor-associated macrophages and inflammatory pathways, contributing to resistance and disease recurrence. Although PIM inhibitors have demonstrated promise in preclinical studies, their clinical translation has been limited by toxicity and resistance mechanisms. Emerging evidence suggests that combining PIM inhibition with immune checkpoint blockade may synergistically enhance anti-tumor efficacy. These editorial highlights the promising therapeutic strategy of inhibiting PIM kinases to reshape the immune microenvironment in prostate cancer, thereby improving the efficacy of immunotherapy.