Abstract
Toll-like receptor (TLR) 4 is expressed on normal and malignant prostate epithelial cells. The TLR4 and its downstream signaling pathways mediate innate immune responses in the host against invading pathogens. However, multiple lines of evidence shows that TLR4 expression is increased in prostate tissues from prostate cancer patients, and altered TLR4 signals may promote cancer development, as well as antitumor effects. In this review, we have summarized key features of the TLR4 signaling pathway and its associated immune responses and focused on the pathologic role of TLR4 in prostate carcinogenesis and tumor progression.
Highlights
Prostate cancer is one of the most common causes of morbidity and mortality in men
Patients with metastatic prostate cancer have increased plasma IL-6 levels, which are correlated with PSA levels [29]. These results suggest that inflammation such as bacterial infection, prostatitis, and pro-inflammatory cytokines (e.g., IL-6) may play a role in prostate cancer etiology and progression
We hypothesize that persistent bacterial LPS stimulation from bacterial colonization of the prostate may promote the development of immune suppressive microenvironment, including generation of T regulatory cells and tumor-associated macrophages and recruitment of myeloid-derived suppressor cells into local prostate tumor environment through TLR4 signaling
Summary
Prostate cancer is one of the most common causes of morbidity and mortality in men. The prostate surrounds the upper part of the urethra. Inflammation through TLR4 signaling promotes the development of immune suppressive microenvironment, such as recruitment myeloid-derived suppressor cells into local tumor environment, in breast, colon, renal cell, and pancreatic cancers [14,15,16,17,18]. No such evidence has been shown in prostate cancer. We focus on the pathologic role of TLR4 and its effects in prostate cancer development and progression. This is important for therapeutic strategy targeting TLR signaling or responsiveness (e.g., inhibitors for specific pro-inflammatory cytokine) to prevent prostate cancer development and progression
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