Biochemical and Biophysical Research Communications
Regular ArticleInduction of Apoptosis in HL-60 Human Promyelocytic Leukemia Cells by Adenosine A3Receptor Agonists☆
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Translation of nanomedicines from lab to industrial scale synthesis: The case of squalene-adenosine nanoparticles
2019, Journal of Controlled ReleaseAttenuation of Sunitinib-induced cardiotoxicity through the A3 adenosine receptor activation
2017, European Journal of PharmacologyCitation Excerpt :The dose range for Sunitinib (0.1 – 10 μM) and IB-MECA (10 nM – 10 µM) was based from cell viability studies, where these drugs were showing to have an apoptotic effect on HL60 cells. Sunitinib has shown to induced apoptosis in HL60 cells in the dose range of 1–9 µM through G1 cell cycle arrest (Teng et al., 2013), while the study by Kohno et al. (1996) showed that IB-MECA concentrations ≥ 10 µM caused apoptosis in HL-60 cells (Kohno et al., 1996). Sunitinib and IB-MECA were dissolved in DMSO and the DMSO concentration was < 0.05% (v/v) during the in vitro studies.
Mechanism of apoptotosis induced by ortho-topolin riboside in human hepatoma cell line SMMC-7721
2012, Food and Chemical ToxicologyCitation Excerpt :These results suggest that oTR induced SMMC-7721 cancer cell apoptosis by regulating the levels of pro-apoptotic Bax and anti-apoptotic Bcl-2/Bcl-xL proteins. In general, two distinct cytotoxic mechanisms are involved in animal cells, one is the intracellular phosphorylation (Cottam et al., 1993; Lin et al., 1988), the other is extracellular adenosine receptors (Kohno et al., 1996). It has been reported that N6-substituted derivatives of adenosine induced apoptosis was related to the intracellular accumulation of corresponding mononucleotides rather than to their interaction with extracellular adenosine receptors in HL-60 cells (Mlejnek and Dolezel, 2005; Mlejnek and Kuglik, 2000).
Two New Adenosine Derivatives and their Antiproliferative Properties: An In Vitro Evaluation
2022, Anti-Cancer Agents in Medicinal Chemistry
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ADO, adenosine; CADO, 2-chloroadenosine; CGS 21680, 2-[4-[(2-carboxyethyl)-phenyl]ethylamino]-5′N-ethylcarboxamidoadenosine; CI-IB-MECA, N6-(3-iodobenzyl)-2-chloro-adenosine-5′-N-methyluronamide; CPA, N6-cyclopentyladenosine; IB-MECA, N6-(3-iodobenzyl)adenosine-5′-N-methyluronamide; NECA, 5′-N-ethylcarboxamidoadenosine; Tris, tris(hydroxymethyl)]aminomethane; XAC, (8-[4-[[[[(2-aminoethyl)amino]-carbonyl]methyl]oxy]phenyl]-1,3-dipropylxanthine).
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