Inhibition of interferon-γ-activated nuclear factor-κB by cyclosporin A: a possible mechanism for synergistic induction of apoptosis by interferon-γ and cyclosporin A in gastric carcinoma cells

2003 ◽  
Vol 305 (4) ◽  
pp. 797-805 ◽  
Author(s):  
Kiichiro Beppu ◽  
Takashi Morisaki ◽  
Hisashi Matsunaga ◽  
Akihiko Uchiyama ◽  
Eikichi Ihara ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Cyclosporin A ◽  
Nuclear Factor Κb ◽  
Interferon Γ ◽  
Carcinoma Cells ◽  
Nuclear Factor ◽  
Synergistic Induction ◽  
Induction Of Apoptosis

scholarly journals Parthenolide and sulindac cooperate to mediate growth suppression and inhibit the nuclear factor-κB pathway in pancreatic carcinoma cells

2005 ◽  
Vol 4 (4) ◽  
pp. 587-594 ◽  
Author(s):  
Michele T. Yip-Schneider ◽  
Harikrishna Nakshatri ◽  
Christopher J. Sweeney ◽  
Mark S. Marshall ◽  
Eric A. Wiebke ◽  
...  
Keyword(s):  
Pancreatic Carcinoma ◽  
Nuclear Factor Κb ◽  
Growth Suppression ◽  
Carcinoma Cells ◽  
Nuclear Factor

scholarly journals Imatinib enhances docetaxel-induced apoptosis through inhibition of nuclear factor-κB activation in anaplastic thyroid carcinoma cells

Thyroid ◽  
2012 ◽  
pp. 120406132503004
Author(s):  
EunSook Kim ◽  
Michiko Matsuse ◽  
Vladimir Saenko ◽  
Keiji Suzuki ◽  
Akira Ohtsuru ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Nuclear Factor Κb ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Nuclear Factor ◽  
Induced Apoptosis

Inhibition of Nuclear Factor κB Activation Attenuates Apoptosis Resistance in Lymphoid Cells

Blood ◽  
1998 ◽  
Vol 91 (12) ◽  
pp. 4624-4631 ◽  
Author(s):  
I. Jeremias ◽  
C. Kupatt ◽  
B. Baumann ◽  
I. Herr ◽  
T. Wirth ◽  
...  
Keyword(s):  
Cell Lines ◽  
Nuclear Factor Κb ◽  
Lymphoid Cells ◽  
Nuclear Factor ◽  
Apoptosis Induction ◽  
Apoptosis Resistance ◽  
Anticancer Treatment ◽  
Induction Of Apoptosis ◽  
Transient Overexpression ◽  
Factor Α

Death-inducing ligands (DILs) such as tumor necrosis factor α (TNFα) or the cytotoxic drug doxorubicin have been shown to activate a nuclear factor κB (NFκB)-dependent program that may rescue cells from apoptosis induction. We demonstrate here that TRAIL (TNF-related apoptosis-inducing ligand), a recently identified DIL, also activates NFκB in lymphoid cell lines in a kinetic similar to TNFα. NFκB activity is independent from FADD, caspases, and apoptosis induction. To study the influence of NFκB activity on apoptosis mediated by TRAIL, CD95, TNFα, or doxorubicin, NFκB activation was inhibited using the proteasome inhibitor N-acetyl-L-leucinyl-L-leucinyl-L-norleucinal or transient overexpression of mutant IκBα. Sensitivity for induction of apoptosis was markedly increased by these treatments in apoptosis sensitive cell lines. Moreover, both in cell lines and in primary leukemia cells that are resistant towards induction of apoptosis by DILs and doxorubicin, antagonization of NFκB activity partially restored apoptosis sensitivity. These data suggest that inhibition of NFκB activation may provide a molecular approach to increase apoptosis sensitivity in anticancer treatment.

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