Tanshinone IIA inhibits acute promyelocytic leukemia cell proliferation and induces their apoptosis in vivo

2016 ◽  
Vol 56 (1) ◽  
pp. 46-52 ◽  
Author(s):  
Kaiji Zhang ◽  
Jian Li ◽  
Wentong Meng ◽  
Hongyun Xing ◽  
Yiming Yang
Keyword(s):  
Cell Proliferation ◽  
Acute Promyelocytic Leukemia ◽  
Leukemia Cell ◽  
Promyelocytic Leukemia ◽  
Tanshinone Iia ◽  
Acute Promyelocytic Leukemia Cell

Ruthenium metallodendrimers with anticancer potential in an acute promyelocytic leukemia cell line (HL60)

2017 ◽  
Vol 87 ◽  
pp. 39-47 ◽  
Author(s):  
Sylwia Michlewska ◽  
Maksim Ionov ◽  
Dzmitry Shcharbin ◽  
Marta Maroto-Díaz ◽  
Rafael Gomez Ramirez ◽  
...  
Keyword(s):  
Cell Line ◽  
Acute Promyelocytic Leukemia ◽  
Leukemia Cell ◽  
Promyelocytic Leukemia ◽  
Leukemia Cell Line ◽  
Acute Promyelocytic Leukemia Cell ◽  
Promyelocytic Leukemia Cell Line

Synergic effects of arsenic trioxide and cAMP during acute promyelocytic leukemia cell maturation subtends a novel signaling cross-talk

Blood ◽  
2002 ◽  
Vol 99 (3) ◽  
pp. 1014-1022 ◽  
Author(s):  
Qi Zhu ◽  
Ji-Wang Zhang ◽  
Hai-Qing Zhu ◽  
Yu-Lei Shen ◽  
Maria Flexor ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Arsenic Trioxide ◽  
Acute Promyelocytic Leukemia ◽  
Cross Talk ◽  
Fusion Gene ◽  
Leukemia Cell ◽  
Promyelocytic Leukemia ◽  
Dependent Manner ◽  
Induced Differentiation

Abstract Acute promyelocytic leukemia (APL) is characterized by the specific chromosome translocation t(15;17) with promyelocytic leukemia-retinoic acid receptor-α (PML-RARA) fusion gene and the ability to undergo terminal differentiation as an effect of all-trans retinoic acid (ATRA). Recently, arsenic trioxide (As2O3) has been identified as an alternative therapy in patients with both ATRA-sensitive and ATRA-resistant APL. At the cellular level, As2O3 triggers apoptosis and a partial differentiation of APL cells in a dose-dependent manner; both effects are observed in vivo among patients with APL and APL animal models. To further explore the mechanism of As2O3-induced differentiation, the combined effects of arsenic and a number of other differentiation inducers on APL cell lines (NB4 and NB4-R1) and some fresh APL cells were examined. The data show that a strong synergy exists between a low concentration of As2O3 (0.25 μM) and the cyclic adenosine monophosphate (cAMP) analogue, 8-CPT-cAMP, in fully inducing differentiation of NB4, NB4-R1, and fresh APL cells. Furthermore, cAMP facilitated the degradation of As2O3-mediated fusion protein PML-RARα, a process considered to play a key role in overcoming the differentiation arrest of APL cells. On the other hand, cAMP could significantly inhibit cell growth by modulating several major players in G1/S transition regulation. Interestingly, H89, an antagonist of protein kinase A, could block the differentiation-inducing effect of As2O3potentiated by cAMP. These results thus support the existence of a novel signaling cross-talk for APL maturation, which may deepen understanding of As2O3-induced differentiation in vivo, and thus furnish insights for new therapeutic strategies.

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