Abstract | Prostate cancer (PC) is a leading cause of death in men. Inflammation is one of the initiating processeswhereby cells are trafficked into the tumor microenvironment by specific cytokines termed chemokines. Thisrecruitment is complex and involves diverse leukocyte subsets with procancer and anticancer functions.Chemokines promote/abrogate proliferation of cancerous cells, block/aid apoptosis, and are instrumental/detrimental in cancer cell migration required for metastasis. Chemokines guide the release/transport ofimmune cells that serve aschaperones at sites of inflammation, and after subsequent activation, theylead toan immune response. The variety of immune cells recruited at the site of tumor initiation possess uniquefunctions, and the plethora of chemokines released by each cell derived from a progenitor cell activatedunder a defined set of conditions dictates its specific role in cancer progression/regression. Geographicconsequences that govern the climate and endemic diseases, along with the associated evolutionaryeffects that at times protect populations from one disease, could lead to genetic variations that determine arole for ethnicity and race in PC risk and susceptibility. Dysregulated expression or an imbalance in thehomeostatic mechanisms associated with chemokines is implicated in PC. This review discusses the role of inflammation and chemokines in PC. |
---|