Aspartate-Based Inhibitor of Interleukin-1β-Converting Enzyme Prevents Antitumor Agent-Induced Apoptosis in Human Myeloid Leukemia U937 Cells

Mashima, Tetsuo; Naito, Mikihiko; Kataoka, Satoshi; Kawai, Hidehiko; Tsuruo, Takashi

doi:10.1006/bbrc.1995.1584

Cited by 148 publications

(99 citation statements)

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“…In contrast to the study by Khwaja et al, 6 it was reported that the death of U937 cells in response to antiFas, TNF and etoposide treatment was blocked by caspase inhibitors. 40,41 We have repeated these experiments and confirmed that while zVAD-fmk effectively blocked the DNA fragmentation, the total percentage of annexin V positive cells (including both 7AAD positive and negative) was unaltered following etoposide or anti-Fas treatment (data not shown). Likewise, when U937 cells were examined in a 4 day MTT growth assay, caspase inhibition did not spare the cells from the death or anti-proliferative effects of antiFas or etoposide treatment.…”

Section: Nuclear Changes and Phosphatidylserine Translocation In Thesmentioning

confidence: 79%

Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis

Wilson

Browning

2002

Cell Death Differ

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The HT29 adenocarcinoma is a common model of epithelial cell differentiation and colorectal cancer and its death is an oftanalyzed response to TNF family receptor signaling. The death event itself remains poorly characterized and here we have examined the involvement of caspases using pan-caspase inhibitors. zVAD-fmk did not block death of HT29 cells in response to activation of the Fas, TRAIL, TNF, TWEAK and LTb receptors. The secondary induction of TNF or the other known bona fide death inducing ligands did not account for death following LTb receptor activation indicating that TNF family receptors can trigger a caspase-independent death pathway regardless of the presence of canonical death domains in the receptor. To provide a frame of reference, the phenotype of HT29 death was compared to four other TNF family receptor triggered death events; Fas induced Jurkat cell apoptosis, TNF/zVAD induced L929 fibroblast necrosis, TNF induced death of WEHI 164 fibroblastoid cells and TNF/zVAD induced U937 death. The death of HT29 and U937 cells under these conditions is an intermediate form with both necrotic and apoptotic features. The efficient coupling of TNF receptors to a caspase-independent death event in an epithelial cell suggests an alternative approach to cancer therapy.

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Section: Nuclear Changes and Phosphatidylserine Translocation In Thesmentioning

confidence: 79%

Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis

Wilson

Browning

2002

Cell Death Differ

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“…Paclitaxel, camptothecin, etoposide, adriamycin and cyclosporin A were obtained from Sigma (St. Louis, MO). An inhibitor for caspases, z-Asp-CH 2 -DCB, 33) was purchased from Peptide Institute (Osaka). The Fas antibody (ZB4) and the neutralizing FasL antibody (NOK-2) were obtained from Medical and Biological Laboratories (Nagoya) and Pharmingen (San Diego, CA), respectively.…”

Section: Methodsmentioning

confidence: 99%

Bcl‐2 Inhibits Calcineurin‐mediated Fas Ligand Expression in Antitumor Drug‐treated Baby Hamster Kidney Cells

Simizu

Shibasaki

Osada

2000

Japanese Journal of Cancer Research

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It is well known that human leukemia cells, such as HL-60 and U937 are sensitive to antitumor drugs, but human normal lung fibroblasts, such as WI-38 cells are resistant to the drugs. However, the mechanisms of the different responses to apoptosis in these cell lines remain unclear. We report here that an increase of Fas and Fas ligand (FasL) expression was required for antitumor druginduced apoptosis in WI-38 and baby hamster kidney (BHK) cells, but not in HL-60 cells. Then, we used BHK cells transfected with the bcl-2 gene to investigate the involvement of complex formation of Bcl-2 and calcineurin. Calcineurin was imported to the nucleus in response to the drug treatment. Overexpression of Bcl-2 and cyclosporin A treatment inhibited the nuclear import and FasL expression, and as a result, both inhibited apoptosis. Although a caspase inhibitor, z-Asp-CH 2 -DCB, suppressed the drug-induced apoptosis, it failed to inhibit the drug-induced expression of Fas and FasL. These findings suggest that initially the Fas/FasL system is activated by calcineurindependent transcription followed by activation of the downstream caspase cascade resulting in antitumor drug-induced apoptosis in BHK cells, but not in HL-60 cells. Furthermore, Bcl-2 inhibits the nuclear import of calcineurin and suppresses calcineurin-mediated FasL expression during antitumor drug-induced apoptosis.

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“…This result suggests that DXR-and GSH-DXR-induced DNA fragmentation occur via activation of caspase-3, but not of caspase-1. Several reports have described that anthracycline was able to induce inter-nucleosomal DNA fragmentation in treated cells (Kaufmann et al, 1993;Bose et al, 1995;Yamashita et al, 1995;Chen et al, 1996;Mizushima et al, 1996), but the magnitude of the process induced by GSH-DXR treatment was markedly more potent than that induced by DXR.…”

Section: Inhibition Of Apoptosis By Caspase Inhibitormentioning

confidence: 98%

Caspase-3 activation during apoptosis caused by glutathione–doxorubicin conjugate

et al. 1999

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Glutathione–doxorubicin (GSH–DXR) effectively induced apoptosis in rat hepatoma cells (AH66) at a lower concentration than DXR. After 24 h of drug treatment, DNA fragmentation of the cells was observed at the concentration of 1.0 μ M DXR or 0.01 μ M GSH–DXR. Increase in caspase-3 activity and DNA fragmentation were observed within 12 h and 15 h after treatment with either drug. Intracellular caspase-3 activity was increased in a dose-dependent manner after treatment with DXR or GSH–DXR, and caspase-3 activity correlated well with the ability to induce DNA fragmentation. When the cells were treated with either DXR or GSH–DXR for only 6 h, apoptotic DNA degradation and caspase-3 activation occurred 24 h after treatment. DNA fragmentation caused by these drugs was prevented completely by simultaneous treatment with the caspase-3 inhibitor, acetyl–Asp–Glu–Val–Asp-aldehyde (DEVD-CHO), at 10 μ M . By contrast, DNA fragmentation was not prevented by the caspase-1 inhibitor, acetyl–Tyr–Val–Ala–Asp–aldehyde (YVAD-CHO), at the same concentration as DEVD-CHO, and caspase-1 was not activated at all by the treatment of AH66 cells with both DXR and GSH–DXR. These results demonstrate that DXR and GSH–DXR induce apoptotic DNA fragmentation via caspase-3 activation, but not via caspase-1 activation, and that GSH–DXR enhances the activation of caspase-3 approximately 100-fold more than DXR. Moreover, the findings suggested that an upstream apoptotic signal that can activate caspase-3 is induced within 6 h by treating AH66 cells with the drug. © 1999 Cancer Research Campaign

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Aspartate-Based Inhibitor of Interleukin-1β-Converting Enzyme Prevents Antitumor Agent-Induced Apoptosis in Human Myeloid Leukemia U937 Cells

Cited by 148 publications

References 0 publications

Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis

Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis

Bcl‐2 Inhibits Calcineurin‐mediated Fas Ligand Expression in Antitumor Drug‐treated Baby Hamster Kidney Cells

Caspase-3 activation during apoptosis caused by glutathione–doxorubicin conjugate

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