Apoptosis Induced by Adenosine in Human Leukemia HL-60 Cells

Tanaka, Yasuharu; Yoshihara, Koichiro; Tsuyuki, Motokatsu; Kamiya, Tomoya

doi:10.1006/excr.1994.1196

Cited by 91 publications

(73 citation statements)

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“…This effect of Ado for DNA fragmentation was progressively increased as time dependently as shown in Figure 1A. In these data, we demonstrated that Ado induces DNA fragmentation as a time-and dose-dependent manner, and these findings are supported by previous other reports (Kizaki et al, 1990;Tanaka et al, 1994;Wakade et al ., 1994; Abbrachio e t a l., 1995). The percentages of DNA fragmentation were analyzed by the modified diphenylamine method described in methods.…”

Section: R E S U L T S Adenosine Induces Apoptosis In Hl-60 Cellssupporting

confidence: 92%

“…Its intracellular increase in such diseases leads an idea that an Ado transporter might play an important role in the entrance of Ado into the cells (Kizaki et al, 1990;Abbrachio et al, 1995). However, several lines of evidence suggest that Ado-induced apoptosis was mediated by Ado specific membrane-bound receptors, like its other functions (Tanaka et al, 1994;Wakade et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

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Active adenosine transporter-mediated adenosine entrance into HL-60 cells leads to the induction of apoptosis through down-regulation of c-Myc

Hong

Jeong²,

Ahn³

et al. 1997

Exp Mol Med

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Section: R E S U L T S Adenosine Induces Apoptosis In Hl-60 Cellssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Active adenosine transporter-mediated adenosine entrance into HL-60 cells leads to the induction of apoptosis through down-regulation of c-Myc

Hong

Jeong²,

Ahn³

et al. 1997

Exp Mol Med

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“…HL-60 cells induced to undergo apoptosis by adenosine or cytochalasin B also appear more dispersed than untreated cells. 12 HL-60 cells in cultures treated with nbl antisense oligomers appeared almost evenly dispersed like a monolayer on the bottom of the well. To investigate whether this apparent attachment to the matrix modulated cell death induced by nbl antisense oligomers, we examined the effect of incubating oli-…”

Section: Suppression Of Nbl Expression and Apoptotic Induction By Act Dmentioning

confidence: 99%

“…This cell line was used as a model system in view of its high constitutive nbl expression 6 and because its morphological changes under various apoptosis-inducing conditions have been well-studied. 1,6,11,12 HL-60 cells were transfected with a plasmid comprising of nbl cDNA sequences cloned in antisense orientation into the pMSG vector (pMSGanti-nbl). This vector allows DEX-inducible, MMTV LTRdriven expression of cloned sequences and has been used for Relationship between levels of residual nbl mRNA and DNA fragmentation.…”

Section: Suppression Of Nbl Expression and Apoptotic Induction By Act Dmentioning

confidence: 99%

Antisense sequences of the nbl gene induce apoptosis in the human promyelocytic leukemia cell line HL-60

et al. 1998

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Apoptosis is induced by the transcriptional inhibitor actinomycin D (Act D) in various cell types, particularly many leukemic cell lines such as HL-60. A common feature of these cell lines is their high constitutive expression level of the nbl gene, which was originally isolated by virtue of its abundance in a Namalwa Burkitt lymphoma cDNA library. In contrast, cell lines which constitutively express nbl at low levels appear not to undergo typical apoptotic death in response to Act D. Apoptotic induction by Act D in cells which normally express nbl at high levels was found in this study to be closely associated with a decline in nbl mRNA levels, raising the possibility that apoptosis could be induced by lowering nbl expression levels in such cells. Transient expression of nbl antisense sequences in HL-60 cells decreased cell viability, and induced typical apoptotic morphology such as cell shrinkage, chromatin condensation and nuclear fragmentation. Incubation with nbl antisense oligomers also induced similar features in HL-60 cells and in another high nbl-expressing cell line, Jurkat, but had little effect in HepG2 cells which constitutively express nbl at low levels. These findings suggest that lowering constitutively high levels of nbl expression can induce apoptosis.

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“…Part of this effect may be attributed to adenosine via the activation of ARs and sustained increase in cAMP levels [5]. Besides the activation of extracellular receptors [11,[15][16][17], direct intracellular toxicity (also by adenosine metabolites) has been described [18][19][20][21]. Furthermore, adenosine is able to stimulate cell growth and proliferation and/or to induce apoptosis in various normal and tumor cell lines.…”

Section: Introductionmentioning

confidence: 99%

Antiproliferative effects of selective adenosine receptor agonists and antagonists on human lymphocytes: evidence for receptor-independent mechanisms

Schiedel

Lacher

Linnemann

et al. 2013

Purinergic Signalling

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The effects of standard adenosine receptor (AR) agonists and antagonists on the proliferation of human T lymphocytes, unstimulated and phytohemagglutininstimulated human peripheral blood lymphocytes (PBL), and Jurkat T cells were investigated. Real-time PCR measurements confirmed the presence of all four AR subtypes on the investigated cells, although at different expression levels. A 2A ARs were predominantly expressed in PBL and further upregulated upon stimulation, while malignant Jurkat T cells showed high expression levels of A 1 , A 2A , and A 2B ARs. Cell proliferation was measured by [ 3 H]-thymidine incorporation assays. Several ligands, including the subtype-selective agonists CPA (A 1 ), BAY60-6583 (A 2B ), and IB-MECA (A 3 ), and the antagonists PSB-36 (A 1 ), MSX-2 (A 2A ), and PSB-10 (A 3 ) significantly inhibited cell proliferation at micromolar concentrations, which were about three orders of magnitude higher than their AR affinities. In contrast, further investigated AR ligands, including the agonists NECA (nonselective) and CGS21680 (A 2A ), and the antagonists preladenant (SCH-420814, A 2A ), PSB-1115 (A 2B ), and PSB-603 (A 2B ) showed no or only minor effects on lymphocyte proliferation. The anti-proliferative effects of the AR agonists could not be blocked by the corresponding antagonists. The non-selective AR antagonist caffeine stimulated phytohemagglutinin-activated PBL with an EC 50 value of 104 μM. This is the first study to compare a complete set of commonly used AR ligands for all subtypes on lymphocyte proliferation. Our results strongly suggest that these compounds induce an inhibition of lymphocyte proliferation and cell death through AR-independent mechanisms.

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Apoptosis Induced by Adenosine in Human Leukemia HL-60 Cells

Cited by 91 publications

References 0 publications

Active adenosine transporter-mediated adenosine entrance into HL-60 cells leads to the induction of apoptosis through down-regulation of c-Myc

Active adenosine transporter-mediated adenosine entrance into HL-60 cells leads to the induction of apoptosis through down-regulation of c-Myc

Antisense sequences of the nbl gene induce apoptosis in the human promyelocytic leukemia cell line HL-60

Antiproliferative effects of selective adenosine receptor agonists and antagonists on human lymphocytes: evidence for receptor-independent mechanisms

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