The role of platelets in
cancer development and progression is increasingly evident, and several platelet-
cancer interactions have been discovered, including the uptake of platelet microparticles (PMPs) by
cancer cells. PMPs inherit a myriad of
proteins and small RNAs from the parental platelets, which in turn can be transferred to
cancer cells following internalization. However, the exact effect this may have in
acute myelogenous leukemia (AML) is unknown. In this study, we sought to investigate whether PMPs could transfer their contents to the THP-1 cell line and if this could change the biological behavior of the recipient cells. Using
acridine orange stained PMPs, we demonstrated that PMPs were internalized by THP-1 cells, which resulted in increased levels of miR-125a, miR-125b, and miR-199. In addition, co-incubation with PMPs protected THP-1 and primary AML cells against
daunorubicin-induced cell death. We also showed that PMPs impaired cell growth, partially inhibited cell cycle progression, decreased mitochondrial membrane potential, and induced differentiation toward macrophages in THP-1 cells. Our results suggest that this altering of cell phenotype, in combination with decrease in cell activity may offer resistance to
daunorubicin-induced apoptosis, as serum
starvation also yielded a lower frequency of dead and apoptotic cells when treated with
daunorubicin.