FIGURE 2.

KLF11-mediated down-regulation of cPLA2α-PGE₂ inhibit cell proliferation.A, to test the cell biological significance of the cPLA2α-PGE₂ pathway, FLO cells were treated for 48 h with 30 μm arachidonic acid, a catalytic product of cPLA2α, and increased proliferation by 22 ± 2.6%, whereas AACOCF3, a cPLA2α inhibitor, decreased proliferation by 39.5 ± 0.4% compared with control (BrdUrd incorporation, p < 0.05). The effect of AACOCF3α on FLO cell proliferation was reversed by the catalytic product of cPLA2α namely arachidonic acid and PGE₂. Similar results were noted using other esophageal cancer cells (SKGT-4 and BE-HGD). These findings support that the effect of cPLA2α on cell proliferation is mediated by the release of arachidonic acid and production of PGE₂. B–D, compared with EV, adenoviral infection of FLO (multiplicity of infection 30), SEG-1 (multiplicity of infection 100), and SKGT-4 (multiplicity of infection 100) cells for 48 h with KLF11 significantly (p < 0.05) reduced BrdUrd incorporation in cells that were treated with vehicle (49.5 ± 4.7, 38.5 ± 1.6, and 40 ± 5.9%, respectively for FLO, SEG-1 cells, and SKGT-4, p < 0.05), however, this growth inhibitory effect of KLF11 was abrogated in the cells that were treated with 30 μm arachidonic acid (AA, a catalytic product of cPLA2α and substrate of PGE₂) or 2 ng/ml of PGE₂ suggesting that the growth inhibitory effect of KLF11 is mediated via down-regulation of cPLA2α-PGE2 pathway.