Tumor necrosis factor alpha (TNFα) can trigger both cell survival and apoptosis. In the present study, from the flow cytometry results, we found that the prolonged-treatment of TNFα until 24 h, resulted apoptosis in AM-1 cells (ameloblastoma cell line). These results were confirmed by DAPI staining, which showed nuclear fragmentation feature of AM-1 cells under treatment of TNFα. Our further investigation using specific caspase inhibitors showed that caspase-3 played a crucial role in mediating TNFα-induced apoptosis in AM-1 cells. In addition, significant elevation of TNFα potential in inducing apoptosis was seen by applying LY294002, phosphatidylinositol-3-OH kinase (PI3K) inhibitor, or U0126, mitogen-activated extracellular-regulated kinase (MEK1/2) inhibitor, prior to the treatment of TNFα in AM-1 cells. These results suggested that TNFα induced both cell survival and apoptosis pathways in ameloblastoma and potential of TNFα in inducing apoptosis can be improved by inhibiting TNFα-induced Akt and p44/42 mitogen-activated protein kinase (MAPK) cell survival pathways.
|Number of pages||7|
|Publication status||Published - Jan 2006|
All Science Journal Classification (ASJC) codes
- Oral Surgery
- Cancer Research