Procaspase-3 and its active large subunit localized in both cytoplasm and nucleus are activated following application of apoptotic stimulus in Ramos-Burkitt lymphoma B cells

An, Sungkwan; Park, Myungjin; Park, In-Chul; Hong, Seok‐Il; Knox, Kirstine A.

doi:10.3892/ijmm.12.3.311

Cited by 9 publications

(7 citation statements)

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“…The apoptotic cascade, therefore, might result in transport of the activated form into the nucleus or activation of the nuclear procaspase form. In the Ramos Burkit lymphoma cell line, An et al (2003) observed similar localization patterns for pro-caspase 3; after induction of apoptosis, activated caspase 3 was demonstrated to be present in the nucleus as well as in the cytoplasm. In another model system, pro-caspase 3 was demonstrated to be constitutively nuclear in Jurkat cells (Ramuz et al, 2003).…”

Section: Discussionmentioning

confidence: 63%

Induction of apoptosis involving multiple pathways is a primary response to cyclin A1‐deficiency in male meiosis

Salazar

Joshi

Liu

et al. 2005

Developmental Dynamics

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The meiotic arrest in male mice null for the cyclin A1 gene (Ccna1) was associated with apoptosis of spermatocytes. To determine whether the apoptosis in spermatocytes was triggered in response to the arrest at G2/M phase, as opposed to being a secondary response to overall disruption of spermatogenesis, we examined testes during the first wave of spermatogenesis by terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick end-labeling (TUNEL) staining. We observed enhanced apoptosis coinciding with the arrest point in postnatal day 22 tubules, with no overt degeneration. Along with activation of caspase-3, an increase in the levels and change of subcellular localization of Bax protein was observed in cyclin A1-deficient spermatocytes, which coincided with the detection of apoptosis. As p53 is implicated in the activation of Bax-mediated cell death, we generated mice lacking both cyclin A1 and p53. Although the absence of p53 did not rescue the meiotic arrest, there was a decrease in the number of apoptotic cells in the double-mutant testes. This finding suggested that p53 may be involved in the process by which the arrested germ cells are removed from the seminiferous tubules but that other pathways function as well to ensure removal of the arrested spermatocytes. Developmental Dynamics 234:114 -123, 2005.

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Section: Discussionmentioning

confidence: 63%

Induction of apoptosis involving multiple pathways is a primary response to cyclin A1‐deficiency in male meiosis

Salazar

Joshi

Liu

et al. 2005

Developmental Dynamics

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“…As a central apoptotic effector, it plays a key role in promoting apoptosis [14] . After cleaving caspase-3, the active form of caspase 3 is released, indicating that the caspase 3 proenzyme is activated and has begun to execute its apoptotic function [15] .…”

Section: Discussionmentioning

confidence: 99%

Anti-tumor activity of CrTX in human lung adenocarcinoma cell line A549

et al. 2011

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Aim: To assess the cytotoxic effect of crotoxin (CrTX), a potent neurotoxin extracted from the venom of the pit viper Crotalus durissus terrificus, in human lung adenocarcinoma A549 cells and investigated the underlying mechanisms. Methods: A549 cells were treated with gradient concentrations of CrTX, and the cell cycle and apoptosis were analyzed using a flow cytometric assay. The changes of cellular effectors p53, caspase-3 and cleaved caspase-3, total P38MAPK and pP38MAPK were investigated using Western blot assays. A549 xenograft model was used to examine the inhibition of CrTX on tumor growth in vivo. Results: Treatment of A549 cells with CrTX (25-200 μg/mL) for 48 h significantly inhibited the cell growth in a dose-dependent manner (IC 50 =78 μg/mL). Treatment with CrTX (25 μg/mL) for 24 h caused G1 arrest and induced cell apoptosis. CrTX (25 μg/mL) significantly increased the expression of wt p53, cleaved caspase-3 and phospho-P38MAPK. Pretreatment with the specific P38MAPK inhibitor SB203580 (5 μmol/L) significantly reduced CrTX-induced apoptosis and cleaved caspase-3 level, but G 1 arrest remained unchanged and highly expressed p53 sustained. Intraperitoneal injection of CrTX (10 μg/kg, twice a week for 4 weeks) significantly inhibited A549 tumor xenograft growth, and decreased MVD and VEGF levels. Conclusion: CrTX produced significant anti-tumor effects by inducing cell apoptosis probably due to activation of P38MAPK and caspase-3, and by cell cycle arrest mediated by increased wt p53 expression. In addition, CrTX displayed anti-angiogenic effects in vivo.

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“…HLA-G inhibits CD8 T cell proliferation by inducing T cell apoptosis in CD8 blasts stimulated by PHA (19,26). The induction of apoptosis is mediated by the activation of the Fas pathway, which activates intracellular caspases (32)(33)(34). T cell apoptosis through the Fas pathway requires the recruitment of the cytoplasmic TNFR-associated factor and activation of caspase 8, and then activation of the effector cysteine proteases, caspases 3, 6, and 7.…”

Section: Discussionmentioning

confidence: 99%

Soluble HLA-G Inhibits Cell Cycle Progression in Human Alloreactive T Lymphocytes

Bahri

Hirsch

Josse

et al. 2006

The Journal of Immunology

121

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HLA-G is involved in regulating T cell responses. Various mechanisms have been proposed to explain the inhibition of T cell proliferation. In this context, the possible role of HLA-G in cell cycle regulation remains to be explored. Using stably transfected M8 cells expressing the secreted isoform (HLA-G5) of HLA-G, we investigated the role of HLA-G in inducing apoptosis and in controlling the cell cycle of activated T cells. Soluble HLA-G (HLA-G5) inhibited both CD4 and CD8 T cell proliferation. However, HLA-G5 did not induce T cell apoptosis, as determined by 3,3′-diethyloxacarbocyanine and propidium iodine labeling. It induced accumulation of the retinoblastoma protein, but not its phosphorylated and active form. Treatment of activated T cells with HLA-G5 also reduced the amounts of cyclin D2, E, A, and B by >80%. In contrast, it induced an accumulation of p27kip, but not p21cip, in activated T cells. HLA-G does not induce apoptosis of alloreactive T cells, but induces p27kip1 and inhibits cell cycle progression.

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Procaspase-3 and its active large subunit localized in both cytoplasm and nucleus are activated following application of apoptotic stimulus in Ramos-Burkitt lymphoma B cells

Cited by 9 publications

References 0 publications

Induction of apoptosis involving multiple pathways is a primary response to cyclin A1‐deficiency in male meiosis

Induction of apoptosis involving multiple pathways is a primary response to cyclin A1‐deficiency in male meiosis

Anti-tumor activity of CrTX in human lung adenocarcinoma cell line A549

Soluble HLA-G Inhibits Cell Cycle Progression in Human Alloreactive T Lymphocytes

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