Potential mechanisms of resistance to TRAIL/Apo2L-induced apoptosis in human promyelocytic leukemia HL-60 cells during granulocytic differentiation

Shiiki, Kazuhiko; Yoshikawa, Hideshi; Kinoshita, Hirokazu; Takeda, Masayuki; Ueno, Akira; Nakajima, Yasuo; Tasaka, Kachio

doi:10.1038/sj.cdd.4400727

Cited by 33 publications

(23 citation statements)

References 42 publications

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“…Although TPA has the ability to decrease intracellular GSH in U937 monocytes, this ability was not observed following TPA-induced differentiation (20). Similarly, the resistance to apoptosis by other cytotoxic agents among differentiated myeloid cells was also reported in other studies (16,17,33). These findings indicate that there may be factors other than intracellular GSH involved in the resistance to arsenic-induced apoptosis of TPA-treated U937 macrophages, under certain circumstances.…”

Section: Discussionsupporting

confidence: 49%

N-acetyl-L-cysteine reduces arsenite-induced cytotoxicity through chelation in U937 monocytes and macrophages

Ghani

Khan

Koriyama

et al. 2014

Molecular Medicine Reports

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Abstract. In the present study, in order to clarify the preventive mechanism of N-acetyl-L-cysteine (NAC) on arsenite-induced apoptosis in U937 cells, which lack functional p53, the cytotoxicity among U937 cells [monocytes and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated macrophages] receiving NAC treatment at different times post arsenite treatment was examined. TPA-treated macrophages were more resistant to arsenite-induced apoptosis than monocytes, which may be associated with the induction of Bcl-2 expression. Pretreatment with 20 mM NAC prior to arsenite exposure suppressed apoptosis up to 75% in the monocytes and 100% in the macrophages. However, 6-h NAC pretreatment and subsequent washing out of NAC from the culture medium prior to arsenite treatment did not inhibit the arsenite-induced apoptosis. Post-treatment by NAC up to 1 h following arsenite exposure almost completely inhibited the cytotoxic effects of arsenite in U937 monocytes and macrophages. The results of the current study indicate that the preventive mechanism of NAC on arsenite-induced apoptosis in U937 monocytes and macrophages mainly involves chelation of arsenite in culture medium.

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Section: Discussionsupporting

confidence: 49%

N-acetyl-L-cysteine reduces arsenite-induced cytotoxicity through chelation in U937 monocytes and macrophages

Ghani

Khan

Koriyama

et al. 2014

Molecular Medicine Reports

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“…In fact, U-937 cells treated with TPA for 14 -24 h already express differentiation markers, and the toxicity of As 2 O 3 was also decreased by preincubation with other differentiation inducers, namely bryostatin 1, sodium butyrate, and VD3. The resistance of differentiated myeloid cells to apoptosis induction by diverse cytotoxic agents has been also documented by other authors (11,(52)(53)(54). Because differentiation and apoptosis are alternative, mutually excluding pathways (55), a restraint in apoptosis may be expected once the differentiation program has been executed.…”

Section: Resultsmentioning

confidence: 84%

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

Fernández

Ramos

Sancho

et al. 2004

Journal of Biological Chemistry

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Arsenic trioxide (As 2 O 3 ) caused apoptosis in U-937 human promonocytic cells. This effect was potentiated by the simultaneous addition of the glutathione (GSH) synthesis inhibitor DL-buthionine-(R,S)-sulfoximine or the protein kinase C activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and bryostatin 1. In addition TPA decreased the intracellular GSH content, caused ERK activation, and potentiated the As 2 O 3 -provoked activation of p38 and JNK. The addition of N-acetyl-L-cysteine, the PKC inhibitor GF109203X, and the MEK/ERK inhibitors PD98059 and U0126 attenuated both apoptosis induction and GSH decrease, whereas the p38 inhibitor SB203580 and the JNK inhibitor SP600125 were ineffective. TPA also potentiated ERK activation and GSH depletion when added simultaneously to cadmium chloride (CdCl 2 ) and doxorubicin. However, TPA only enhanced apoptosis in the case of CdCl 2 , which is a GSH-sensitive agent, whereas it reduced the toxicity of doxorubicin and other DNA-specific drugs. Finally, preincubation for 14 -24 h with TPA did not potentiate but, instead, attenuated the As 2 O 3 -and CdCl 2 -provoked apoptosis. The same result was obtained by preincubation with bryostatin 1 and other differentiation inducers. It is concluded that TPA increases the apoptotic action of As 2 O 3 , an effect mediated by ERK activation and GSH depletion. However, the increase in apoptosis is only effective in non-differentiated cells.

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“…LBH589 induced cell cycle arrest and apoptosis of multiple myeloma cells, the latter involving both caspase-dependent and caspase-independent pathways. Furthermore, gene expression results uncovered a group of proteins, such as Aven (16) and Toso (17)(18)(19), which may play a relevant role in multiple myeloma apoptosis.…”

Section: Introductionmentioning

confidence: 99%

The Histone Deacetylase Inhibitor LBH589 Is a Potent Antimyeloma Agent that Overcomes Drug Resistance

et al. 2006

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Multiple myeloma represents an incurable disease, for which development of new therapies is required. Here, we report the effect on myeloma cells of LBH589, a new hydroxamic acidderived histone deacetylase inhibitor. LBH589 was a potent antimyeloma agent (IC 50 < 40 nmol/L) on both cell lines and fresh cells from multiple myeloma patients, including cells resistant to conventional chemotherapeutic agents. In addition, LBH589 potentiated the action of drugs, such as bortezomib, dexamethasone, or melphalan. Using gene array, quantitative PCR, and Western analyses, we observed that LBH589 affected a large number of genes involved in cell cycle and cell death pathways. LBH589 blocked cell cycle progression, and this was accompanied by p21, p53, and p57 upregulation. LBH589 induced cell death through an increase in the mitochondrial outer membrane permeability. LBH589 favored apoptosome formation by inducing cytochrome c release, Apaf-1 up-regulation, and caspase-9 cleavage. In addition, LBH589 stimulated a caspase-independent pathway through the release of AIF from the mitochondria. LBH589 down-regulated Bcl-2 and particularly Bcl-X. Moreover, overexpression of Bcl-X in multiple myeloma cells prevented LBH589-induced cell death. All these data indicate that LBH589 could be a useful drug for the treatment of multiple myeloma patients. (Cancer Res 2006; 66(11): 5781-9)

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Potential mechanisms of resistance to TRAIL/Apo2L-induced apoptosis in human promyelocytic leukemia HL-60 cells during granulocytic differentiation

Cited by 33 publications

References 42 publications

N-acetyl-L-cysteine reduces arsenite-induced cytotoxicity through chelation in U937 monocytes and macrophages

N-acetyl-L-cysteine reduces arsenite-induced cytotoxicity through chelation in U937 monocytes and macrophages

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

The Histone Deacetylase Inhibitor LBH589 Is a Potent Antimyeloma Agent that Overcomes Drug Resistance

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