Priming with GM-CSF instead of G-CSF enhances CAG-induced apoptosis of acute monocytic leukemia cells in vitro

2019 ◽  
Vol 84 (2) ◽  
pp. 265-273
Author(s):  
Meiqing Lei ◽  
Limin Liu ◽  
Depei Wu
Keyword(s):  
Leukemia Cells ◽  
Acute Monocytic Leukemia ◽  
Monocytic Leukemia ◽  
Gm Csf ◽  
Induced Apoptosis

Human Monocytoid Leukemia Cells Are Highly Sensitive to Apoptosis Induced by 2′-Deoxycoformycin and 2′-Deoxyadenosine: Association With dATP-Dependent Activation of Caspase-3

Blood ◽  
1998 ◽  
Vol 92 (9) ◽  
pp. 3368-3375 ◽  
Author(s):  
Nozomi Niitsu ◽  
Yuri Yamaguchi ◽  
Masanori Umeda ◽  
Yoshio Honma
Keyword(s):  
Cell Lines ◽  
Caspase 3 ◽  
Lymphoma Cell ◽  
Leukemia Cells ◽  
Acute Monocytic Leukemia ◽  
U937 Cells ◽  
Monocytic Leukemia ◽  
Low Concentrations ◽  
American Society ◽  
Induced Apoptosis

Abstract The adenosine deaminase (ADA) inhibitor 2′-deoxycoformycin (dCF) significantly inhibits the proliferation of leukemia and lymphoma cell lines. When cells were incubated in the presence of both dCF and 2′-deoxyadenosine (dAd), the concentration of dCF required to induce apoptosis of monocytoid leukemia cells was much lower than that required for myeloid, erythroid, or lymphoma cell lines. Among the cell lines tested, U937 cells were the most sensitive to this treatment. The concentration of dCF that effectively inhibited the proliferation of U937 cells was 1/1,000 of that required for lymphoma cell lines, on a molar basis. However, the uptake of dCF or dAd in U937 cells was comparable with that in other leukemia and lymphoma cell lines. The intracellular accumulation of dATP in U937 cells was only slightly higher than that in other leukemia cells in dCF-treated culture. Treatment with dCF plus dAd induced apoptosis in U937 cells at low concentrations, and this apoptosis was reduced by treatment with caspase inhibitors. Induction of caspase-3 (CPP32) activity accompanied the apoptosis induced by dCF plus dAd. No activation of CPP32 was observed in cytosol prepared from exponentially growing leukemia and lymphoma cells. However, dATP effectively induced CPP32 activation in cytosol from monocytoid cells, but not in that from nonmonocytoid cells, suggesting that dATP-dependent CPP32 activation is at least partly involved in the preferential induction of apoptosis in monocytoid leukemia cells. The combination of dCF and dAd may be useful for the clinical treatment of acute monocytic leukemia. © 1998 by The American Society of Hematology.

scholarly journals Dihydroartemisinin-induced apoptosis in human acute monocytic leukemia cells

2017 ◽  
Author(s):  
Jia‑Tian Cao ◽  
Hui‑Min Mo ◽  
Yue Wang ◽  
Kai Zhao ◽  
Tian‑Tian Zhang ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Acute Monocytic Leukemia ◽  
Monocytic Leukemia ◽  
Induced Apoptosis

Human Monocytoid Leukemia Cells Are Highly Sensitive to Apoptosis Induced by 2′-Deoxycoformycin and 2′-Deoxyadenosine: Association With dATP-Dependent Activation of Caspase-3

Blood ◽  
1998 ◽  
Vol 92 (9) ◽  
pp. 3368-3375 ◽  
Author(s):  
Nozomi Niitsu ◽  
Yuri Yamaguchi ◽  
Masanori Umeda ◽  
Yoshio Honma
Keyword(s):  
Cell Lines ◽  
Caspase 3 ◽  
Lymphoma Cell ◽  
Leukemia Cells ◽  
Acute Monocytic Leukemia ◽  
U937 Cells ◽  
Monocytic Leukemia ◽  
Low Concentrations ◽  
American Society ◽  
Induced Apoptosis

The adenosine deaminase (ADA) inhibitor 2′-deoxycoformycin (dCF) significantly inhibits the proliferation of leukemia and lymphoma cell lines. When cells were incubated in the presence of both dCF and 2′-deoxyadenosine (dAd), the concentration of dCF required to induce apoptosis of monocytoid leukemia cells was much lower than that required for myeloid, erythroid, or lymphoma cell lines. Among the cell lines tested, U937 cells were the most sensitive to this treatment. The concentration of dCF that effectively inhibited the proliferation of U937 cells was 1/1,000 of that required for lymphoma cell lines, on a molar basis. However, the uptake of dCF or dAd in U937 cells was comparable with that in other leukemia and lymphoma cell lines. The intracellular accumulation of dATP in U937 cells was only slightly higher than that in other leukemia cells in dCF-treated culture. Treatment with dCF plus dAd induced apoptosis in U937 cells at low concentrations, and this apoptosis was reduced by treatment with caspase inhibitors. Induction of caspase-3 (CPP32) activity accompanied the apoptosis induced by dCF plus dAd. No activation of CPP32 was observed in cytosol prepared from exponentially growing leukemia and lymphoma cells. However, dATP effectively induced CPP32 activation in cytosol from monocytoid cells, but not in that from nonmonocytoid cells, suggesting that dATP-dependent CPP32 activation is at least partly involved in the preferential induction of apoptosis in monocytoid leukemia cells. The combination of dCF and dAd may be useful for the clinical treatment of acute monocytic leukemia. © 1998 by The American Society of Hematology.

scholarly journals Interleukin-5 (IL-5) increases spontaneous apoptosis of B-cell chronic lymphocytic leukemia cells in vitro independently of bcl-2 expression and is inhibited by IL-4

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2297-2304 ◽  
Author(s):  
T Mainou-Fowler ◽  
VA Craig ◽  
JA Copplestone ◽  
MD Hamon ◽  
AG Prentice
Keyword(s):  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
Percentage Increase ◽  
Spontaneous Apoptosis ◽  
Interleukin 5 ◽  
The Third ◽  
The Mean ◽  
Induced Apoptosis ◽  
Cell Chronic Lymphocytic Leukemia

Abstract During hematopoiesis, viability factors that suppress apoptosis are required throughout the differentiation process. Some of these factors may also function as growth factors. Interleukin-5 (IL-5) is recognized as a growth factor in hematopoiesis. We examined the involvement of IL- 5 as a viability factor of B-CLL in vitro. In 13 B-CLL cases studied, IL-5 at 20 U/mL increased spontaneous apoptosis by a mean percentage of 53% (range, 20% to 129%) (P < .05) after 2 days in culture. On the third day, the mean percentage increase was 37% (range, 18% to 50%). In all cases, IL-4 protected B-CLL cells against IL-5-induced apoptosis by a mean percentage of 47% (range, 18% to 81%) (P < .001). This protection was specific to IL-4 and it was reduced with anti-IL-4 antibody. In addition, expression of bcl-2 protein in untreated cultures was not significantly different from that of the IL-5-treated cells; mean equivalent of soluble fluorochrome (MESF) was 5.2 (range, 3.0 to 6.8) and 4.9 (range, 3.0 to 6.3), respectively (P > .2). In freshly isolated B-CLL cells, the MESF was 4.5 (range, 2.4 to 6.6). These results show that IL-5 induced apoptosis in B-CLL cells by a pathway that is independent of bcl-2 expression. IL-4 partially protects against this effect.

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