Tetraarsenictetrasulfide and Arsenic Trioxide Exert Synergistic Effects on Induction of Apoptosis and Differentiation in Acute Promyelocytic Leukemia Cells

Wang, Shuping; Zhou, Min; Ouyang, Jian; Geng, Zhirong; Wang, Zhilin

doi:10.1371/journal.pone.0130343

Cited by 19 publications

(13 citation statements)

References 42 publications

(64 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The definitive molecular mechanism was inducing proliferation/apoptosis‐related differential protein expression profile in NB4 cells (Liu et al, ; Qi et al, ; Wang et al, ). As 4 S 4 also arrested NB4 cell growth in the G2/M phase (Lu et al, ; Wang, Zhou, Ouyang, Geng, & Wang, ). To our knowledge, the role of As 4 S 4 in enhancing apoptosis in immune cells has not been described.…”

Section: Discussionmentioning

confidence: 99%

Tetra-arsenic tetra-sulfide ameliorates lupus syndromes by inhibiting IL-17 producing double negative T cells

Zhao

Cai

et al. 2019

Dermatologic Therapy

View full text Add to dashboard Cite

Systemic lupus erythematosus (SLE) is an autoimmune disease of uncertain etiology that affects multiple tissues and organs. Tetra‐arsenic tetra‐sulfide (As4S4), a traditional Chinese medicine, is effective on acute promyelocytic leukemia with mild side effects. In our previous study, BXSB lupus‐prone mice treated with As4S4 has showed improved monocytosis, decreased serum interleukin (IL)‐6 and suppressed skin, liver and renal lesions with well‐tolerance. In this study, we explored the effect and mechanism of As4S4 on the MRL/lpr mice. MRL/lpr and wild MRL/MpJ mice were divided into control and As4S4 treatment groups and dosed with As4S4 or placebo for 8 weeks. We found that As4S4 prevented the skin, renal and lung lesions of MRL/lpr mice. As4S4 significantly decreased the double negative T (DN T) cells and reduced the serum levels of IL‐17, IL‐10, and antinuclear antibodies titer. Further results revealed that the FasL was decreased, and activated caspases elevated in DN T cells in As4S4 treated MRL/lpr mice. Taken together, As4S4 could selectively suppresses DN T cells by inducing apoptosis. It also reduced inflammatory cytokines IL‐17, which may be produced by DN T cells. As4S4 may represent a new therapy for SLE.

show abstract

Section: Discussionmentioning

confidence: 99%

Tetra-arsenic tetra-sulfide ameliorates lupus syndromes by inhibiting IL-17 producing double negative T cells

Zhao

Cai

et al. 2019

Dermatologic Therapy

View full text Add to dashboard Cite

show abstract

“…Apoptosis is triggered by two pathways; one is the death receptor-mediated extrinsic pathway, and the other is the mitochondrial-dependent intrinsic pathway (17,18). Bcl-2 family members are key components of the mitochondrial-dependent intrinsic apoptosis pathway (19). Bcl-2 family members are classified into three subgroups: The pro-apoptotic proteins, including Bax and Bak; the anti-apoptotic proteins, including Bcl-2, myeloid cell leukemia-1 and Bcl-extra large; and the BH3-only proteins, including BH3 interacting domain death agonist, p53 upregulated modulator of apoptosis and Noxa (20).…”

Section: Discussionmentioning

confidence: 99%

Solanine induced apoptosis and increased chemosensitivity to Adriamycin in T-cell acute lymphoblastic leukemia cells

Xing

Wang

et al. 2018

Oncol Lett

View full text Add to dashboard Cite

Solanine is an alkaloid and is the main extract of the traditional Chinese herb, . It has been reported that Solanine has anti-inflammatory and antitumor properties. The present study aimed to investigate the antitumor effect of Solanine in Jurkat cells and demonstrate the molecular mechanism of antitumor activity of Solanine. A Cell Counting Kit-8 assay demonstrated that Solanine inhibited the proliferation of Jurkat cells in a dose-and time-dependent manner. Cell apoptosis was measured by flow cytometry. Flow cytometry revealed that Solanine induced apoptosis in a dose-dependent manner in Jurkat cells. Reverse transcription-quantitative polymerase chain reaction demonstrated that Solanine modulated the mRNA levels of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax). Additionally, Bcl-2 and Bax expression was measured using western blot analysis. Western blot analysis revealed a significant increase in the expression of Bax and decrease in the expression of Bcl-2. Solanine increased the chemosensitivity of Jurkat cells to Adriamycin. In summary, the present results indicated that the antitumor activity of Solanine was associated with inhibition of cell proliferation, induction of apoptosis and increasing cytotoxicity of Adriamycin. Therefore, Solanine may have potential as a novel agent for the treatment of acute lymphocytic leukemia.

show abstract

“…Despite the toxicity of arsenic, arsenic trioxide has been used in a number of traditional Chinese medicines, and has been used to treat cancer ( 13 ). Previous studies have identified that ATO induces apoptosis in acute promyelocytic leukemia (APL) cells ( 14 , 15 ), glioblastoma cells ( 16 ) and gastric cancer cells ( 17 ), and inhibits cell growth in breast cancer ( 18 ). The use of ATO is also being evaluated for the treatment of certain malignancies, including lung cancer ( 19 ), hepatocellular cancer ( 20 ) and basal cell cancer ( 21 ).…”

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide induces the apoptosis and decreases NF‑κB expression in lymphoma cell lines

Zhong

Chen

2018

Oncol Lett

View full text Add to dashboard Cite

Lymphoma is a type of cancer that develops from certain immune system cells. Arsenic trioxide (ATO) has attracted wide attention owing to its antitumor activities. However, the role of ATO in tumorigenesis and progression remains to be investigated. In the present study, the antitumor function of ATO was investigated in in lymphoma Raji and Jurkat cell lines and the effect of ATO on nuclear factor (NF)-κB expression levels. A Cell Counting kit-8 assay was used to assess cellular proliferation and the degree of cell apoptosis was measured by flow cytometric analysis; these assays demonstrated that ATO inhibited proliferation and promoted the apoptosis of Raji and Jurkat cells in a dose- and time-dependent manner. Western blot analysis revealed that ATO treatment affected the expression of apoptosis-associated proteins by downregulating the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2) and upregulating the pro-apoptotic protein Bcl-2-associatedX and the degree of caspase-3 cleavage. In addition, reverse transcription-quantitative polymerase chain reaction and western blot analysis showed that the mRNA and protein expression levels of NF-κB were downregulated significantly following treatment with 2 µM ATO for 24, 48 and 72 h in the two cell lines. Additionally, immunofluorescence staining indicated that NF-κB expression diminished following ATO treatment in a time-dependent manner. These data indicated that ATO inhibited the proliferation of lymphoma cells by inducing cell apoptosis, which may be associated with the inhibition of the NF-κB signaling pathway. The findings of the present study may lay the foundation for developing a personalized medicine strategy using ATO via targeting of the NF-κB signaling pathway in lymphoma.

show abstract

Tetraarsenictetrasulfide and Arsenic Trioxide Exert Synergistic Effects on Induction of Apoptosis and Differentiation in Acute Promyelocytic Leukemia Cells

Cited by 19 publications

References 42 publications

Tetra-arsenic tetra-sulfide ameliorates lupus syndromes by inhibiting IL-17 producing double negative T cells

Tetra-arsenic tetra-sulfide ameliorates lupus syndromes by inhibiting IL-17 producing double negative T cells

Solanine induced apoptosis and increased chemosensitivity to Adriamycin in T-cell acute lymphoblastic leukemia cells

Arsenic trioxide induces the apoptosis and decreases NF‑κB expression in lymphoma cell lines

Contact Info

Product

Resources

About