Acidic leucine-rich nuclear phosphoprotein 32 family member B (ANP32B) contributes to retinoic acid-induced differentiation of leukemic cells

2012 ◽  
Vol 423 (4) ◽  
pp. 721-725 ◽  
Author(s):  
Yun Yu ◽  
Shao-Ming Shen ◽  
Fei-Fei Zhang ◽  
Zhao-Xia Wu ◽  
Bin Han ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Family Member ◽  
Leukemic Cells ◽  
Induced Differentiation ◽  
Nuclear Phosphoprotein

Adenanthin Upregulates c/ebp β Expression with Induction of Differentiation of the ATRA-Sensitive and -Resistant leukemic Cells.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1602-1602
Author(s):  
Ying-Li Wu ◽  
Chuan-Xu Liu ◽  
Guo-Qiang Chen
Keyword(s):  
Retinoic Acid ◽  
Vitamin D3 ◽  
Retinoic Acid Receptor ◽  
Promyelocytic Leukemia ◽  
Leukemic Cells ◽  
Monocytic Differentiation ◽  
Induced Differentiation ◽  
Nb4 Cells ◽  
Protein Levels ◽  
Short Period

Abstract Application of all-trans retinoic acid (ATRA) has significantly improved the outcome of patients with acute promyelocytic leukemia (APL), a unique subtype of acute myeloid leukemia (AML) characterized with the reciprocal translocation t(15;17) that results in the expression of leukemia-promoting promyelocytic leukemia-retinoic acid receptor-α (PML-RARα) protein. However, most patients usually relapsed in a short period and followed by generation of retinoid resistance. Therefore, it is imperative to explore agents to overcome the resistance. In this work, we found that adenanthin, a diterpenoid compound extracted from medicinal herbs, could induce monocytic differentiation of ATRA-sensitive APL-derived NB4 cells. Especially, the differentiation-inducing effect could also be seen in the agent-treated ATRA-resistant NB4-LR1, NB4-LR2 cells, as evidenced by the morphology and the increased expression of cell surface differentiation antigens CD11b and CD14. Based on this discovery, we also found that adenanthin significantly upregulated the expression of CCAAT enhancer–binding protein beta (C/EBPβ), but not the C/EBPα and C/EBPε at its transcription and protein levels, which was accompanied by the activation of c-Jun N-terminal kinases signal pathway. On the other hand, silence of C/EBPβ by specific small-interfering RNA abrogated the adenanthin induced differentiation in NB4 cells. All these data proposed the role of C/EBPβ in adenanthin induced differentiation. Furthermore, we investigated the potential combinational effects of the natural compound with other known differentiation-inducing agents including ATRA and 1, 25-dihydroxy vitamin D3. The results demonstrated that adenanthin strikingly enhanced ATRA (10nM) induced granulocyte differentiation and 1, 25-dihydroxy vitamin D3 (1nM) induced monocytic differentiation. These results suggest that adenanthin may be a potential antileukemia agent for the ATRA-sensitive and -resistant APL and deserves to be further investigated in the future.

NDRG1 contributes to retinoic acid-induced differentiation of leukemic cells

2009 ◽  
Vol 33 (8) ◽  
pp. 1108-1113 ◽  
Author(s):  
Su Chen ◽  
Yu-Hui Han ◽  
Ying Zheng ◽  
Meng Zhao ◽  
Hua Yan ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Leukemic Cells ◽  
Induced Differentiation

Variable Regulation of Sensitivity to Retinoic Acid-induced Differentiation in Wild-type and Retinoic Acid-resistant HL-60 Cells

1989 ◽  
Vol 1 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Robert E. Gallagher ◽  
Fernando de Cuevillas ◽  
Chin-Sen Chang ◽  
Edward L. Schwartz
Keyword(s):  
Retinoic Acid ◽  
Wild Type ◽  
Induced Differentiation

Cell cycle analysis during retinoic acid induced differentiation of a human embryonal carcinoma-derived cell line

1987 ◽  
Vol 20 (2-3) ◽  
pp. 153-160 ◽  
Author(s):  
Christine L. Mummery ◽  
Marga A. van Rooijen ◽  
Stieneke E. van den Brink ◽  
Siegfried W. de Laat
Keyword(s):  
Cell Cycle ◽  
Retinoic Acid ◽  
Cell Line ◽  
Embryonal Carcinoma ◽  
Cell Cycle Analysis ◽  
Induced Differentiation

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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