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Titolo:
Arsenic trioxide-induced apoptosis and differentiation are associated respectively with mitochondrial transmembrane potential collapse and retinoic acid signaling pathways in acute promyelocytic leukemia
Autore:
Cai, X; Shen, YL; Zhu, Q; Jia, PM; Yu, Y; Zhou, L; Huang, Y; Zhang, JW; Xiong, SM; Chen, SJ; Wang, ZY; Chen, Z; Chen, GQ;
Indirizzi:
Shanghai Second Med Univ, Rui Jin Hosp, Shanghai Inst Hematol, Shanghai 200025, Peoples R China Shanghai Second Med Univ Shanghai Peoples R China 200025 Peoples R China
Titolo Testata:
LEUKEMIA
fascicolo: 2, volume: 14, anno: 2000,
pagine: 262 - 270
SICI:
0887-6924(200002)14:2<262:ATAADA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-LINES; RAR-ALPHA; DOWN-REGULATION; NUCLEAR-BODIES; NB4 CELLS; IN-VITRO; PML; AS2O3; TRANSLOCATION; T(15-17);
Keywords:
arsenic trioxide; apoptosis; differentiation; mitochondrial transmembrane potentials; retinoic acid receptor; sulfhydryl group;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Chen, GQ Shanghai Second Med Univ, Rui Jin Hosp, Shanghai Inst Hematol, 197 Rui JinRd 2, Shanghai 200025, Peoples R China Shanghai Second Med Univ 197 Rui Jin Rd 2 Shanghai Peoples R China 200025
Citazione:
X. Cai et al., "Arsenic trioxide-induced apoptosis and differentiation are associated respectively with mitochondrial transmembrane potential collapse and retinoic acid signaling pathways in acute promyelocytic leukemia", LEUKEMIA, 14(2), 2000, pp. 262-270

Abstract

Recent studies showed that arsenic trioxide (As2O3) could induce apoptosisand partial differentiation of leukemic promyelocytes. Here, we addressed the possible mechanisms underlying these two different effects. 1.0 mu M As2O3-induced apoptosis was associated with condensation of the mitochondrialmatrix, disruption of mitochondrial transmembrane potentials (Delta psi m)and activation of caspase-3 in acute promyelocytic leukemia (APL) cells regardless of their sensitivity to all-trans retinoic acid (ATRA). All these effects were inhibited by dithiothreitol (DTT) and enhanced by buthionine sulfoximine (BSO). Furthermore, BSO could also render HL60 and U937 cells, which had the higher cellular catalase activity, sensitive to As2O3-induced apoptosis. Surprisingly, 1.0 mu M As2O3 did not induce the Delta psi m collapse and apoptosis, while 0.1 mu M As2O3 induced partial differentiation offresh BM cells from a de novo APL patient. In this study, we also showed that 0.2 mM DTT did not block low-dose As2O3-induced NB4 cell differentiation, and 0.1 similar to 0.5 mu M As2O3 did not induce differentiation of ATRA-resistant NB4-derived sublines, which were confirmed by cytomorphology, expression of CD11b, CD33 and CD14 as well as NET reduction. Another interesting finding was that 0.1 similar to 0.5 mu M As2O3 could also induce differentiation-related changes in ATRA-sensitive HL60 cells. However, the differentiation-inducing effect could not be seen in ATRA-resistant HL60 sublineswith RAR alpha mutation. Moreover, low-dose As2O3 and ATRA yielded similargene expression profiles in APL cells. These results encouraged us to hypothesize that As2O3 induces APL cell differentiation through direct or indirect activation of retinoic acid receptor-related signaling pathway(s), while Delta psi m collapse is the common mechanism of As2O3-induced apoptosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 00:50:52