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An Anti‐apoptotic Role of NF‐ κ B in TNF α ‐induced Apoptosis in an Ameloblastoma Cell Line
Author(s) -
Hendarmin Laifa,
Kawano Shintaro,
Yoshiga Daigo,
Sandra Ferry,
Mitsuyasu Takeshi,
Nakao Yu,
Higuchi Yoshinori,
Nakamura Norifumi,
Nakamura Seiji
Publication year - 2008
Publication title -
oral science international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.256
H-Index - 13
eISSN - 1881-4204
pISSN - 1348-8643
DOI - 10.1016/s1348-8643(08)80013-4
Subject(s) - apoptosis , nf κb , tumor necrosis factor alpha , ameloblastoma , cell culture , microbiology and biotechnology , nfkb1 , biology , iκbα , cancer research , cell , necrosis , immunocytochemistry , chromosomal translocation , transcription factor , chemistry , endocrinology , biochemistry , anatomy , maxilla , genetics , gene
Nuclear factor‐ κ B (NF‐ κ B) is involved in the promotion of cell survival in a variety of cell types. The present study focused on the role of NF‐ κ B in TNF α ‐induced apoptosis in an ameloblastoma. Immunohistochemical staining revealed p65 NF‐ κ B protein to be expressed in ameloblastoma tissues. Furthermore, immunoblotting and immunocytochemistry analyses showed that the stimulation of TNF α in an ameloblastoma cell line (AM‐1) induced p65 NF‐ κ B translocation from the cytoplasm to the nucleus, indicating NF‐ κ B activation. These findings were confirmed by an NF‐ κ B luciferase reporter assay, which detected enhanced NF‐ κ B transcription activity of AM‐1 cells by TNF α stimulation. Moreover, pretreatment with SN50, a nuclear translocation inhibitor, prior to TNF α stimulation, effectively inhibited TNF α ‐induced NF‐ κ B activation in AM‐1 cells. In order to reveal the role of NF‐ κ B activation during TNF α ‐induced apoptosis in AM‐1 cells, an apoptosis assay was performed, and showed that the potential of TNF α in inducing apoptosis in AM‐1 cells was significantly elevated by inhibiting the NF‐ κ B activation. These results suggest that NF‐ κ B plays an anti‐apoptotic role in TNF α ‐induced apoptosis in AM‐1 cells.