Neutrophils are short-lived leukocytes and major components of the innate immune 
system. They are key players in the body's defense against pathogens, but their 
contribution to tumor growth and metastasis is controversial. Nevertheless, 
improving the functions of neutrophils in cancer patients, particularly in those 
undergoing chemotherapy, is of clinical significance. In this study, we 
investigated the ability of the immunoreactive fragment of the polypeptide 
prothymosin alpha (proTα), i.e., the decapeptide proTα(100-109), to enhance the 
functions of neutrophils isolated from the peripheral blood of breast cancer 
patients in comparison with those from healthy donors. Activation of neutrophils 
from both groups with proTα(100-109) significantly increased phagocytosis and 
the production of intracellular reactive oxygen species (ROS) compared to 
controls. The release of extracellular ROS and oxidative burst of 
proTα(100-109)-stimulated neutrophils were less improved. Most importantly, upon 
activation with proTα(100-109), neutrophils from breast cancer patients showed 
significantly enhanced cytotoxicity against tumor cell targets. Using a 
scrambled peptide as a control, we showed that the proTα(100-109)-induced 
effects were sequence-specific and comparable to those exerted by the parental 
molecule proTα. The responsiveness of neutrophils to proTα(100-109) or intact 
proTα did not correlate with the tumor grade or other established tumor 
characteristics. Our results suggest that proTα(100-109) activates neutrophils, 
particularly those derived from breast cancer patients, and these effects could 
potentially be used to improve some functions of neutrophils in the clinical 
setting.