PMPs induce tumor cell apoptosis and inhibit tumor growth via miR-24. (A) The indicated number of PMPs collected from freshly isolated human platelets was coincubated with 5 × 10⁴ LLC cells every 24 hours. Cells were counted at 60 hours (n = 8). (B) MC-38 cells, treated as assessed as in panel A (n = 3). (A-B) *P < .0007; **P < .001; ***P < .05; #P < .02; ##P < .01. (C) A total of 5 × 10⁴ LLC cells were transfected and treated every 24 hours with 10⁹ freshly isolated PMPs as indicated, and counted daily (n = 5). (D) MC-38 cells transfected, treated, and analyzed as in panel C. (C-D): *P < .03; **P < .04 (n = 3). (E) LLC cells treated as in panel C were harvested and lysates were processed for western blotting with antibodies to cleaved caspase-3 (cl. cas-3) and β-actin. (F) Lysates of MC-38 cells treated as in panel D were processed for western blotting as in panel E (n = 5) for panels E-F. (G) A total of 1 × 10⁶ LLCs were transfected as indicated, and after 18 hours were seeded as allografts by bolus injection into the flanks of WT mice. Beginning at day 8, 1 × 10¹⁰ PMPs freshly isolated from human platelets were counted and transfused daily by tail vein injection. Tumor volumes were measured daily with calipers (n = 6). *P < .02. (H) MC-38 cells were transfected and implanted, followed by PMP transfusion, and tumor growth was monitored as in panel G. **P < .003 (n = 6). All plots, shown ± SEM. n.s., not significant.