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

14 Citations (Scopus)

Abstract

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
Volume42
Issue number1
DOIs
Publication statusPublished - Jan 2006

All Science Journal Classification (ASJC) codes

  • Oral Surgery
  • Oncology
  • Cancer Research

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