Abstract
| Lingua originale | English |
|---|---|
| pagine (da-a) | 272-279 |
| Numero di pagine | 8 |
| Rivista | Chemotherapy |
| Volume | 51 |
| Stato di pubblicazione | Published - 2005 |
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All Science Journal Classification (ASJC) codes
- Oncology
- Infectious Diseases
- Pharmacology (medical)
- Drug Discovery
- Pharmacology
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Induction of apoptosis by the adenosine derivative IB-MECA in parental or multidrug-resistant HL-60 leukemia cells: possibile relationship to the effects on inhibitor of apoptosis protein levels. / D'Alessandro, Natale; Meli, Maria; Labbozzetta, Manuela; Notarbartolo Di Villarosa, Monica; Poma, Paola; Cervello, Melchiorre.
In: Chemotherapy, Vol. 51, 2005, pag. 272-279.Risultato della ricerca: Article
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TY - JOUR
T1 - Induction of apoptosis by the adenosine derivative IB-MECA in parental or multidrug-resistant HL-60 leukemia cells: possibile relationship to the effects on inhibitor of apoptosis protein levels
AU - D'Alessandro, Natale
AU - Meli, Maria
AU - Labbozzetta, Manuela
AU - Notarbartolo Di Villarosa, Monica
AU - Poma, Paola
AU - Cervello, Melchiorre
PY - 2005
Y1 - 2005
N2 - Background: The effects of the A3 adenosine receptor (A3AR) agonist lB-MECA were examined in HL-60 leukemia and in its multidrug-resistant variant HL60R cells. Methods: Cytotoxicity was evaluated by MTS assays and apoptosis by flow cytometry analyses of DNA fragmentation and phosphatidylserine exposure. The mRNAs of A3AR and inhlbitor of apoptosis proteins (lAPs) were determined by RT-PCR. Results: A3AR expression was similar in HL-60 and HL-60R cells. At ≥ 100 μM, IB-MECA exhibited strong cytotoxic and apoptotic effects in HL-60, but not in HL-60R cells. This activity was not modified by the A3AR antagonis VUF5574, the P-glycoprotein inhibitor verapamil, the adenosine uptake inhibitor NBTI or the anti Fas antibody Z B4, HL-60R cells showed higher levels of different IAPs than H L-60 cells. lB-MECA 100 μM downregulated HlAP1, NAIP and survivin mRNAs in HL-60, but not in HL-60R cells. Conclusions: The antitumor effects of IB-MECA are not mediated by A3AR in HL-60 cells, where the proapoptotic mechanism of the compound may involve downregulation of lAPs. The resistance of HL-60R cells to lB-MECA may depend on their elevated levels of lAPs.
AB - Background: The effects of the A3 adenosine receptor (A3AR) agonist lB-MECA were examined in HL-60 leukemia and in its multidrug-resistant variant HL60R cells. Methods: Cytotoxicity was evaluated by MTS assays and apoptosis by flow cytometry analyses of DNA fragmentation and phosphatidylserine exposure. The mRNAs of A3AR and inhlbitor of apoptosis proteins (lAPs) were determined by RT-PCR. Results: A3AR expression was similar in HL-60 and HL-60R cells. At ≥ 100 μM, IB-MECA exhibited strong cytotoxic and apoptotic effects in HL-60, but not in HL-60R cells. This activity was not modified by the A3AR antagonis VUF5574, the P-glycoprotein inhibitor verapamil, the adenosine uptake inhibitor NBTI or the anti Fas antibody Z B4, HL-60R cells showed higher levels of different IAPs than H L-60 cells. lB-MECA 100 μM downregulated HlAP1, NAIP and survivin mRNAs in HL-60, but not in HL-60R cells. Conclusions: The antitumor effects of IB-MECA are not mediated by A3AR in HL-60 cells, where the proapoptotic mechanism of the compound may involve downregulation of lAPs. The resistance of HL-60R cells to lB-MECA may depend on their elevated levels of lAPs.
KW - A 3 adenosine receptor, IB-MECA, Apoptosis, Multidrug resistance, Inhibitor of apoptosis proteins
UR - http://hdl.handle.net/10447/21118
M3 - Article
VL - 51
SP - 272
EP - 279
JO - Chemotherapy
JF - Chemotherapy
SN - 0009-3157
ER -