Differentiation inducing effect of arsenic trioxide on the C_6 glioma cells
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Objective To evaluate the differentiation inducing effect of arsenic trioxide on the C_6 glioma cells.Methods The expression of GFAP and C-myc protein of the C_6glioma cells were observed with SP immunohistochemistry,which were induced by arsenic trioxide in different time and different concentration.Results The expression of GFAP of the glioma was significantly increased by low concentration arsenic trioxide(0.5～2.0 μmol/L),and a significant decrease of C-myc protein was demonstrated(P0.05).Conclusion The differentiation of C_6glioma cells could be induced by arsenic trioxide effectively.The malignant degree of glioma is decreased after induced by arsenic trioxide.Keywords:
Arsenic Trioxide
Trioxide
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Objective:To explore the effect of arsenic trioxide on cell apoptosis in HL-60 cells.Methods:DNA(deoxyribonucleic acid) line was detected by gelose electrophresis.Changes of cell nucleus stained by Hoecst 33258 in HL-60 cells treated by arsenic trioxide were studied by fluorescence microscope.The apoptosis were detected by flow cytometry.Results:DNA fragment appeared after HL-60 cells exposed to 10 μmol/L arsenic trioxide from 24 to 48 h;cell nucleus were concentrated and fragmented after HL-60 cells exposed to 10 μmol/L arsenic trioxide for 48 h.Treated with 10 μmol/L arsenic trioxide for 12hours,24 hours and 48 h,the apoptotic rate was (8.5±2.1)%,(12.8±3.4)% and(21.4±5.8)%,respectively,but the apoptotic rate in the negative control group only (1.5±0.5)%(P0.05).Conclusion:Arsenic trioxide can induce apoptosis in HL-60 cells.
Arsenic Trioxide
Trioxide
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Objective To investigate the inhibition effect of arsenic trioxide combined with interferon on the growth of epidermal carcinoma cells at different concentrations and different time in order to select the optimized action time and dose of the combination of the two drugs.Methods Through cell culture with human epidermal carcinoma cells A431 in vitro,the inhibition effects of arsenic trioxide combined with INF at different concentrations on proliferation of A431 cells were detected by MTT.The apoptosis rate and the changes of cell cycle in human A431 cells were detected by FCM.Results The results of MTT showed that arsenic trioxide and INF respectively inhibited the proliferation of A431 cells in a dose-dependent and time-dependent manner.The combination of arsenic trioxide with INF inhibited the growth of A431 cells,and the inhibitory rate of the combination application was significantly higher than that of arsenic trioxide only,there was a significant difference between arsenic trioxide and INF(P0.01).There was a synergistic effect of arsenic trioxide and INF combination application.The synergistic effects of arsenic trioxide and INF on inducing apoptosis of A431 cells was more obvious,as compared with that of using simple arsenic trioxide or INF.Conclusion The arsenic trioxide and INF has inhibition effect on the growth of A431 cells in vitro respectively in a dose-dependent and time-dependent manner.The arsenic trioxide and INF can result in the arrearage of S phase of cell growth,and can increase the ration of S phase,and there is a synergistic effect of arsenic trioxide and INF combination application.The induction effect of arsenic trioxide on apoptosis of A431cells is quite obvious,nut INF can enhance the induction effect of arsenic trioxide on apoptosis of A431cells.
Arsenic Trioxide
A431 cells
Trioxide
MTT assay
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Arsenic Trioxide
MTT assay
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Objective: To explore the effect of arsenic trioxide on cell cycle and apoptosis of K562/A02 cells and its possible mechanism.Methods: Adriamycin(Adr) resistant K562/A02 were treated with arsenic trioxide(non-cytotoxic concentration at 4.0υmol/L,5.0υmol/L) or without arsenic trioxide(control),flow cytometry was used to evaluate apoptosis and cell cycle distribution,and change of the expression level of NF-κBp65 protein in nucleus was detected by western blot.Results: As compared with control arsenic trioxide significantly increased the rate of apoptosis,arrested cells in G0/G1phase and reduced the levels of NF-κBp65 protein in nucleus(allP0.05).Conclusion: The underlying mechanism for arsenic trioxide to promote apoptosis of K562/A02 and suppress cell proliferation lies in its impact on NF-κBp65 protein expression.
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Objective:To investigate the effects of arsenic trioxide and all-trans retinoic acid (ATRA) on ovarian cancer cell line SKOV3 and relative mechanism.Methods:Morphological changesof cells were observed and photoed by inverted microscope. Growth inhibition and cell cycles change of SKOV3 line induced by means of MTT/flow cytometry. Immunocytochemical staining was used to examine the expression of P27.Results:The inhibitive effect of arsenic trioxide (5.0 μmol/L) combined with ATRA(1.0 μmol/L) was obvious and the inhibitive degree was stronger than only arsenic trioxide. Higher concentrations of arsenic trioxide and all-trans retinoic acid up-regulated P27 .Conclusion:The inhibitive effect of arsenic trioxide combined with ATRA is more obvious than either one used separately; G2/M retardation is found by flow cytometry and the effect is enhanced in dose-dependent pattern.The apoptosis mechanism of ovarian cancer cell line SKOV3 is related with up-regulating of P27.
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Objective To study the effect of arsenic trioxide on proliferation,apoptosis,cell cycles and phosphorylation oncogene(PPO) expression in the human melanoma cell line A375.Methods The human melanoma cell line A375 was cultured.MTT assay was used to detect the effect of arsenic trioxide on proliferation, apoptosis and cell cycles of A375 cells at different concentrations.The effects of arsenic trioxide on cell cycle and apoptotic rates were assessed by flow cytometry.The morphological changes of cells were determined by the reverse microscopy after the treatment with arsenic trioxide.The influence of arsenic trioxide on the expressions of PPO in the A375 cells were detected with immunohistochemical method.Results It was confirmed by MTT assay that within the concentration interval of 1~10 μmol/L,as the concentration and exposure time increased,the inhibition ratio of arsenic trioxide on the A375 cells gradually increased.The inhibitory effects of arsenic trioxide on the proliferation of the A375 cells showed a time-and concentration-dependent manner.The growth of the A375 cells were arrested at S stage after treatment with arsenic trioxide with flow cytometry.It could be seen by the reverse microscopy that the typical morphological change of apoptosis occurred in the A375 cells.PPO protein was expressed in the intracytoplasm of the A375 cells.The expression of PPO protein diminished in arsenic trioxide-treated cells compared with the controls.There was difference between the control and the experiment groups(P0.05).Conclusions Arsenic trioxide significantly inhibits the proliferation of the A375 cells and there is a positive correlation between the concentration and effectiveness of the drug.The mechanism of action might be related to the apoptosis resulting from inhibition of PPO expression in the A375 cells.
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OBJECTIVE: To explore the mechanism of arsenic trioxide(As2O3)in the treatment of leukemia. METHODS: 1)The expression of CD11b, cell cycle and apoptosis were investigated by flow cytometry. 2)The mRNA expression of c-myc was showed by RT-PCR. RESULTS: Arsenic trioxide significantly increased CD11b in HL-60 cells, and the expression rate of CD11b increased from (14.5±2.1)% to (35.4±5.7)% after treated by 2.5 μmol/L arsenic trioxide for 90 hours (P0.05), and the percentage of NBT positive cells increased from (10.0±2.1)% to (31.2±3.4)%(P0.05),and mRNA expression of c-myc was reduced significantly. CONCLUSION: Arsenic trioxide increases the cell differentiation in HL-60 cells by reducing mRNA expression of c-myc and increasing the expression of CD11b.
Arsenic Trioxide
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Objective To investigate the effects of arsenic trioxide(As2O3) on the cell proliferation and apoptosis of C6 glioma cells in vitro.Methods The C6 glioma cells were treated by 1,3,5 μ mol/L of As2O3 with different duration and observed under the microscope and electromicroscope.The viability of C6 glioma cells was examined by methyl thiazolyl tetrazolium (MTT) assay,and cell cycle and apoptosis were examined by flow cytometry.Results After treatment of 1,3,5 μ mol/L As2O3,C6 glioma cells were inhibited obviously with a dose- and time-dependent manner (P ＜0.05) by MTT.During flow cytometry,more increasing apoptotic cells were found in different concentration As2O3.Characteristic morphological changes were observed in As2O3 intervention by transmission election microscopy including cell shrinkage,physaliphore,nuclear condensation and apoptosis and so on.Conclusion As2O3 can inhibit the cell proliferation and induce the apoptosis of C6 glioma cells.
Key words:
Glioma; Cell culture techniques; Apoptosis; Arsenic trioxide
Arsenic Trioxide
MTT assay
Viability assay
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Objective:To study the changes of cell cycle phase and cell cycle phase regulation protein during arsenic trioxide induced apoptosis in hepatoma cells,and to explore mechanisms of arsenic trioxide inhibited HCC.Methods:Cultured in vitre,HCC SMMC-7721 were treated 72h with 2μmol/L arsenic trioxide.The cell cycle and apoptosis index were detected by flow cytometry(FCM);the morphological changes were observed by transmission electron microscope.The immunohistochemistry was used to detect the protein expression of p21、cyclin D_1,cyclinA.Results:SMMC-7721 cell cycle was arrested in G_1 and S phase by arsenic trioxide.Compared with control in the course of apoptosis induced by arsenic trioxide p21 protein expressions rose significantly(control:1.128;arsenic trioxide:3.794),while cyclinD_1,cyclinA protein expressions decreased significantly(control 1:3.647,2.833;arsenic trioxide:1.133,1.179).Conclusion:Arsenic trioxide could disturb cell cycle progression of SMMC-7721 and induce apoptosis.The mechanism may relate to that arsenic trioxide up-regulate expression of p21 and down-regulate expression of cyclinD_1,cyclinA.
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Objective:We investigate the inhibition effect on lung cancer cells and measured the variation of survivin expression level after treated with arsenic trioxide in vitro. Our objective is to illuminate the possible mechanism of arsenic trioxide on lung cancer. Methods:Lung cancer cell line-A549 cells were cultured in vitro. Different doses of arsenic trioxide were co-cultured with A549 cells and the terminal concentrations were 0.5, 1.0, 2.0, 4.0μmol/L. Cell viability was counted by trpan-blue staining and cell growth inhibition rate was calculated. After centrifuged for 5 min at the condition of 1 000rpm, the sediments were collected for western blot experiment according to the molecular cloning experiment guideline. In this section, the correlation of survivin expression levels inhibited by arsenic trioxide with survival rate of A459 cells was analyzed. Results:A549 cell growth was markedly inhibited by arsenic trioxide as concentration-and time-dependent manner. The level of survivin expression was sown-regulated by arsenic trioxide and also as concentration-and time-dependent manner. The survivin protein level was negatively correlated with the tumor cell survival rate. Conclusion:A549 cell growth is markedly inhibited by arsenic trioxide in vitro. Arsenic trioxide is an effective agent which can inhibit lung cancer cells through inhibiting survivin expression.
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