Objective To assess the clinical effectiveness and safety of inductive treatment with arsenic trioxide （As203） for acute promyelocytic leukemia （APL）. Methods Randomized controlled trials （RCTs） were identified from MEDLINE （1966 -July, 2005 ）, EMBASE （1984 -July, 2005 ）, The Cochrane Library （ Issue 3, 2005） and CBM- disc （1978 -July, 2005）. The references of eligible studies were handsearched. RCTs of As203 treating for APL were included. Data were evaluated and extracted by two reviewers independently with designed extraction form. RevMan 4. 2.7 software was used for data analysis. Results Six RCTs involving 323 patients were included. Two studies reported that there was no statistical difference between As2O3 group and all-transretinoic acid （ATRA） group in mortality for patients with APL or APL patients with complications of desseminated intiavascular coagulation or cerebra hemorrhage. The pooled result of 4 studies showed that there was no statistical difference with RR 0.98, 95 % CI 0.86 to 1.12 in complete remission （CR） rates between the two groups. The result of one study showed that the CR rate of patients with intravenous injection of As203 in 2 divided dosages with longer injection duration was higher with RR 1.31, 95% CI 0.86 to 1.12 compared with those with a single intravenous injection. Adverse effects in As2O3 group were less than ATRA group. Conclusions Inductive treatment with As2O3 for acute promyelocytic leukeuia has similar mortality and CR with less adverse effects compared with ATRA. More trials of high quality are required.
Objective To observe the effect of a wide range of concentration of arsenic trioxide on hepatoma cell line BEL-7402 with variable duration. Methods The cell activity and morphologic changes were studied after treated with different concentration. The apoptosis were detected by flow cytometry assay and DNA Gel electrophoresis. Results The effect of arsenic trioxide on hepatoma cell lines were dependent on the time and concentration obviously. Hepatoma cells cultured with different concentration presented apoptosis features: i.e. intact cell membrane, chromatin condensation, nucleic fragmentation and apoptotic body formation; flow cytometry analysis showed an arrestment at G2/M phase and a subG1 cell peak, DNA gel electrophoresis showed a marked DNA ladder. Conclusion Arsenic trioxide can obviously inhibit the growth of hepatoma cell lines through inducing hepatoma cell apoptosis.
【Abstract】Objective To study the effects of arsenic trioxide (As2O3) on inhibiting the proliferation of hepatic carcinoma cell lines. Methods To detect the inhibiting rate of As2O3 and other 6 kinds of anticancer drugs (such as, NOV, ADM, MMC, 5-Fu, DDP and CTX) on hepatic carcinoma cell lines BEL-7404 and SMMC-7721 by using MTT assay. Results As compared with other 6 kinds of anticancer drugs, the inhibiting rate of As2O3 was the highest one (P＜0.01 or P＜0.05). The inhibiting rates of As2O3 in the groups with the concentration above 1.0 μg/ml were no different (P＞0.05). Conclusion As2O3 could inhibit hepatic carcinoma cell lines BEL-7404 and SMMC-7721 effectively in vitro. Drug sensitivity tests of different concentration’s As2O3 should be done in order to select the minimal and effective concentration of arsenic trioxide and reduce the side effects of arsenic trioxide.
目的 观察三氧化二砷联合顺铂腔内注射治疗恶性胸腔积液的疗效和毒副反应。 方法 2011年9月－2012年9月，将恶性胸腔积液患者60例，随机分为治疗组和对照组，每组各30例。在胸腔积液充分引流后，治疗组胸腔内注射三氧化二砷20 mg联合顺铂60 mg；对照组只给予胸腔灌注顺铂60 mg，胸腔灌注化学疗法药物两组均1次/周，共3次。观察疗效及不良反应。 结果 治疗组和对照组的有效率分别为93.3%和56.7%（P＜0.05）。治疗组和对照组的一般状况改善率分别为70.0%和40.0%（P＜0.05）。两组的不良反应相近。 结论 三氧化二砷联合顺铂腔内注射治疗恶性胸腔积液具有协同增效作用，不良反应小。
Objective To observe the outcomes of using different concentrations of arsenic trioxide at varying phases on the breast cancer cell line MCF-7 and to study the mechanism of this effect. Methods The effect of arsenic trioxide on the growth of breast cancer cell line MCF-7 was observed after applying arsenic trioxide of different concentrations （0.5-16 μmol/Ｌ）. The inhibitory effect of arsenic trioxide on the cell proliferation was investigated with 3-(4，5-dimethyl-thizazol-2-yl)-2， 5-diphenyl tetrazolium bromide (MTT) and the induction of arsenic trioxide on cell apoptosis was detected by DNA ladder and terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL). Results The effect of arsenic trioxide on breast cancer cell line MCF-7 depended on the phase and the dose. The number of cell decreased significantly and there were conspicuously typical morphological changes of apoptosis after the use of arsenic trioxide， including membrane blebbing， chromatin pyknosis, nuclear fragmentation and the formation of apoptotic body. The typical DNA ladders were observed in the MCF-7 cells after 48 h administration of arsenic trioxide at concentrations 1-8 μmol/Ｌ. Significant elevations of apoptosis index at 24 h, 48 h and 72 h were all detected by TUNEL after incubating with 4 μmol/L arsenic trioxide. Conclusion Arsenic trioxide may inhibit the growth of breast cancer cell line MCF-7 significantly by inducing the apoptosis of breast cancer cell.
【Abstract】ObjectiveTo investigate the effects of As2O3 on expression of NF-κB p65, survivin and caspase-3 in human breast infiltrating duct carcinoma xenograft model on nude mice. Methods A human breast infiltrating duct carcinoma model on nude mice was established and the nude mice were divided randomly into three groups: control group, DDP group and As2O3 group （1.5 and 3.0 mg/kg concentrations）. The expression of survivin mRNA was detected with the method of in situ hybridization and the expressions of NF-κB p65, survivin and caspase-3 protein were measured with immunohistochemistry. ResultsThe positive rates of NF-κB p65 and survivin expression were higher in the control group than those in the DDP group and the As2O3 groups, but that of caspase-3 was on the opposite way (P＜0.01). The positive rates of NF-κB p65 and survivin in As2O3 group were negatively related with the concentrations of As2O3 (P＜0.01), but that of caspase-3 was on the opposite way (P＜0.01). The expressions of NF-κB p65 and survivin protein were positively correlated with that of survivin mRNA, but any of them was negatively correlated with the expression of caspase-3 protein. ConclusionAs2O3 inhibites survivin probably by inhibiting the activity of NFκB p65 and subsequently activates caspase-3, which induces apoptosis of human breast infiltrating duct carcinoma cells and is in a dose-dependent manner.
The article aims to explore the optimal concentration of arsenic trioxide (As2O3) on HepG2 of liver cancer cells, and the effect of As2O3 on the migration, invasion and apoptosis of HepG2 cells. In this study, the activity of HepG2 cells treated with 0, 1, 2, 4, 8, 16, 32 μmol/L As2O3 was tested by CCK-8 method, the semi-inhibitory concentration (IC50) was calculated, and the morphological changes of HepG2 cells were observed after the action of As2O3 at IC50 concentration for 12, 24, 48 h. The effect of As2O3 on cell migration and invasion ability was verified by wound healing experiment and Transwell invasion experiment. Western blot and qRT-PCR were used to detect the effects of As2O3 on the gene and protein expression levels related to cell migration, invasion and apoptosis. The results showed that, compared with the control group, the activity of HepG2 cells decreased with the increase of the concentration of As2O3 treatment, showing a dose-dependent effect, and its IC50 was 7.3 μmol/L. After 24 hours’ treatment with 8 μmol/L As2O3, HepG2 cells underwent significant apoptosis, and its migration and invasion abilities were significantly reduced. In addition, the protein expression levels of RhoA, Cdc42, Rac1 and matrix metalloproteinase-9 (MMP-9) were down-regulated, the protein and mRNA expression levels of anti-apoptotic gene Bcl-2 were significantly down-regulated, and the protein and mRNA expression levels of pro-apoptotic genes Bax and Caspase-3 were significantly up-regulated. The above results indicate that certain concentration of As2O3 can inhibit the migration and invasion of hepatocellular carcinoma cells and promote the apoptosis of hepatocellular carcinoma cells.