Breast cancer represents the most common
malignancy among women in the world. Although immuno-, chemo- and
radiation therapy are widely recognized as the therapeutic trifecta, new strategies in the fight against
breast cancer are continually explored. The local microenvironment around the
tumor plays a great role in
cancer progression and invasion, representing a promising therapeutic target. CCL5 is a potent
chemokine with a physiological role of immune cell attraction and has gained particular attention in R&D for
breast cancer treatment. Its
receptor, CCR5, is a well-known co-factor for HIV entry through the cell membrane. Interestingly, biology research is unusually unified in describing CCL5 as a pro-oncogenic factor, especially in
breast cancer. In silico, in vitro and in vivo studies blocking the CCL5/CCR5 axis show
cancer cells become less invasive and less malignant, and the extracellular matrices produced are less oncogenic. At present, CCR5 blocking is a mainstay of HIV treatment, but despite its promising role in
cancer treatment, CCR5 blocking in
breast cancer remains unperformed. This review presents the role of the CCL5/CCR5 axis and its effector mechanisms, and names the most prominent hurdles for the clinical adoption of anti-CCR5 drugs in
cancer.