ArticleBiochemical pharmacology2002
p53-Independent induction of Fas and apoptosis in leukemic cells by an adenosine derivative, Cl-IB-MECA.
Article in Biochemical pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 58 citations in OpenAlex.
- Multifactoral immune modulation potentiates durable remission in multiple models of aggressive malignancy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Species dependence of APurinergic signalling · 2023Review
- 2‑Cl‑IB‑MECA regulates the proliferative and drug resistance pathways, and facilitates chemosensitivity in pancreatic and liver cancer cell lines.International journal of molecular medicine · 2022Article
- Purine-Metabolising Enzymes and Apoptosis in Cancer.Cancers · 2019Review
- Polypharmacology of NJournal of medicinal chemistry · 2017Article
- Immunity, inflammation and cancer: a leading role for adenosine.Nature reviews. Cancer · 2013Review
- Effects of synthetic A3 adenosine receptor agonists on cell proliferation and viability are receptor independent at micromolar concentrations.Journal of physiology and biochemistry · 2013Article
- The p53-independent induction of apoptosis in breast cancer cells in response to proteasome inhibitor bortezomib.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- Putative role of the adenosine A(3) receptor in the antiproliferative action of N (6)-(2-isopentenyl)adenosine.Purinergic signalling · 2011Article
- Molecular mechanisms of A3 adenosine receptor-induced G1 cell cycle arrest and apoptosis in androgen-dependent and independent prostate cancer cell lines: involvement of intrinsic pathway.Journal of cancer research and clinical oncology · 2011Article
- Functional selectivity of adenosine receptor ligands.Purinergic signalling · 2011Article
- Adenosine A(3) receptor suppresses prostate cancer metastasis by inhibiting NADPH oxidase activity.Neoplasia (New York, N.Y.) · 2009Article
- Adenosine receptors and cancer.Handbook of experimental pharmacology · 2009Review
- Emerging adenosine receptor agonists.Expert opinion on emerging drugs · 2007Review
- The Anti-Cancer Effect of AImmunology, endocrine & metabolic agents in medicinal chemistry · 2007Article
- Modulation of the Akt/Ras/Raf/MEK/ERK pathway by A₃ adenosine receptor.Purinergic signalling · 2006Article
- Adenosine receptors as therapeutic targets.Nature reviews. Drug discovery · 2006Review
- Diisothiocyanate derivatives as potent, insurmountable antagonists of P2Y6 nucleotide receptors.Biochemical pharmacology · 2004Article
- Engineering of ADrug development research · 2003Article
- Tumor necrosis factor alpha-induced apoptosis in astrocytes is prevented by the activation of P2Y6, but not P2Y4 nucleotide receptors.Biochemical pharmacology · 2003Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
A(3) adenosine receptor (A(3)AR) agonists have been reported to influence cell death and survival. The effects of an A(3)AR agonist, 1-[2-chloro-6-[[(3-iodophenyl)methyl]amino]-9H-purin-9-yl]-1-deoxy-N-methyl-beta-D-ribofuranonamide (Cl-IB-MECA), on apoptosis in two human leukemia cell lines, HL-60 and MOLT-4, were investigated. Cl-IB-MECA (> or =30 microM) increased the apoptotic fractions, as determined using fluorescence-activated cell sorting (FACS) analysis, and activated caspase 3 and poly-ADP-ribose-polymerase. Known messengers coupled to A(3)AR (phospholipase C and intracellular calcium) did not seem to play a role in the induction of apoptosis. Neither dantrolene nor BAPTA-AM affected the Cl-IB-MECA-induced apoptosis. Cl-IB-MECA failed to activate phospholipase C in HL-60 cells, while UTP activated it through endogenous P2Y(2) receptors. Induction of apoptosis during a 48hr exposure to Cl-IB-MECA was not prevented by the A(3)AR antagonists [5-propyl-2-ethyl-4-propyl-3-(ethylsulfanylcarbonyl)-6-phenylpyridine-5-carboxylate] (MRS 1220) or N-[9-chloro-2-(2-furanyl)[1,2,4]triazolo[1,5-c]quinazolin-5-yl]benzeneacetamide (MRS 1523). Furthermore, higher concentrations of MRS 1220, which would also antagonize A(1) and A(2A) receptors, were ineffective in preventing the apoptosis. Although Cl-IB-MECA has been shown in other systems to cause apoptosis through an A(3)AR-mediated mechanism, in these cells it appeared to be an adenosine receptor-independent effect, which required prolonged incubation. In both HL-60 and MOLT-4 cells, Cl-IB-MECA induced the expression of Fas, a death receptor. This induction of Fas was not dependent upon p53, because p53 is not expressed in an active form in either HL-60 or MOLT-4 cells. Cl-IB-MECA-induced apoptosis in HL-60 cells was augmented by an agonistic Fas antibody, CH-11, and this increase was suppressed by the antagonistic anti-Fas antibody ZB-4. Therefore, Cl-IB-MECA induced apoptosis via a novel, p53-independent up-regulation of Fas.
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