Priority Research Paper Volume 14, Issue 3 pp 1068—1086

Figure 5. ALOX12 deficient mice are protected from radiation-enhanced tumor colonization. (A) Ten week old C57BL/6NCr mice (n = 3 per condition) were exposed to no irradiation (0 Gy) or 6Gyx5 thoracic IR alone or IR with Rapamycin, INK-128, or ABT-737. Lung tissue was collected at 8 weeks after irradiation (no tumor inoculation). The concentration of 12-LOX protein in lung homogenates was measured by ELISA. (B) SA-β-Galactosidase positive cells were counted in lung tissue collected from C57BL/6J ALOX12^−/− mice at 8 weeks after IR and compared to C57BL/6NCr ALOX12^+/+ mice. (C, D) Ten week old C57Bl/6J ALOX12^−/− mice (n = 10 per condition) were exposed to no irradiation (0 Gy) or 6Gyx5 thoracic IR. Eight weeks after irradiation, 5 × 10⁵ B16F0 cells were injected intravenously via the lateral tail vein. Lung tissue was collected 9 days later to count tumor nodules on the lung surface (C) and to measure the size of tumor foci in the lung (D). (E) B16F10 cells were treated with 12(S)-HETE for a total of 48 hours. BrdU was added to cultures for the last 4 hours prior to assay of BrdU incorporation. (F) B16F0 cells were treated with 12(S)-HETE at the indicated doses and collected for Western blotting at 0–30 minutes.