Inhibition of Akt and MAPK pathways elevated potential of TNFα in inducing apoptosis in ameloblastoma

Ferry Sandra, Laifa Hendarmin, Yu Nakao, Norifumi Nakamura, Seiji Nakamura

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)38-44
Number of pages7
JournalOral Oncology
Issue number1
Publication statusPublished - Jan 2006

All Science Journal Classification (ASJC) codes

  • Oral Surgery
  • Oncology
  • Cancer Research


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