EFFECTS OF ARSENIC TRIOXIDE ON APOPTOSIS AND CELL CYCLE OF HUMAN NASOPHARYNGEAL CARCINOMA CELL LINE
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Objective To investigate the effects of arsenic trioxide (As 2O 3) on the cell cycle and apoptosis of human nasopharyngeal carcinoma cell line. Method Cell morphology, flow cytometry and TUNEL were used to examine the cell apoptosis of human nasopharyngeal carcinoma cell line CNE1 indued by arsenic trioxide.The cell cycle was determined by using flow cytometry. Result Arsenic trioxide induced CNE 1cell apoptosis with typical morphological features, and the apoptotic peak detected by flow cytometric analysis showed a dose-dependent effect. FCM data showed that the G 2/M phase ratios were increased significantly in a dose-dependent manner.Conclusion As 2O 3 could significantly induce CNE1 cell lineapoptosisand alter the cell cycle progression.Keywords:
Arsenic Trioxide
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Objective To study the effects of arsenic trioxide (As 2O 3) on gastric cancer cells in induction of apoptosis.Methods Apoptosis and cell cycle changes of MKN 45 and MKN 28 induced by As 2O 3 were investigated by TUNEL method and flow cytometry.Results After 12 hours of exposure to the drug, MKN 45 and MKN 28 exhibited morphologic features of apoptosis, including cell shrinkage, nuclear condensation, DNA fragmentation and formation of apototic bodies. A typical subdiploid peak before G 0/G 1 phase was observed by flow cytometry. The apoptic index was 7-15% by TUNEL and FACS assay.Conclusions Arsenic trioxide can induce apoptosis of gastric cancer cells and it might have a promising prospect in the treatment of gastric cancer, and worth further studies.
Arsenic Trioxide
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Objective To investigate the possibility of human gastric carcinoma cells apoptosis induced by arsenic trioxide and its mechanism. Methods After treatment with arsenic trioxide,the cytotoxicity to human gastric carcinoma cells MKN45 was quantified using trypan blue exclusion,and IC50 was determined. Apoptotic cells were detected with flow cytometry, DNA cytofluorometry, TUNEL and DNA electrophoresis. Results Arsenic trioxide inhibited the growth of human gastric carcinoma cells MKN45 in a dose dependent manner in a certain range of dose with a IC50 of (11.05±0.25)μmol/L. Apoptotic peak, characteristic morphologic features of apoptosis and DNA ladder were observed in human gastric carcinoma cells MKN45 treated with 10 μmol/L arsenic trioxide. Conclusions Arsenic trioxide can induce apoptosis of human gastric carcinoma cells MKN45, suggesting a great potential treatment of gastric carcinoma.
Arsenic Trioxide
Gastric carcinoma
Trypan blue
IC50
Trioxide
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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 explore the effects of arsenic trioxide(As2O3) on the cell proliferation and expression of Survivin in human epidermal carcinoma cell line-A 431 in vitro.Methods The human epidermal carcinoma cells(cell line A-431) were cultured in vitro,then the cells were treated with different concentrations of arsenic trioxide,then the effects of arsenic trioxide on the cell proliferation of A 431 were detected by MTT,the effects of arsenic trioxide on the cell cycle,apoptosis and expression of Survivin were measured by flow cytometry and the effects of arsenic trioxide on expression of Survivin were also tested by Western Blot.Results The As2O3 could obviously inhibit the proliferation of A 431 cells with concentrations from 10μmol/L to 40μmol/L,which was time-dependent and concentration-dependent.The As2O3 could affect the cell cycle of A 431cells,with the increase of cell counts at G0/G1 phase and the increase of apoptotic cell counts(P0.05).As compared with control group,As2O3 could significantly inhibit the expression of Survivin of A 431 cells.Conclusion The As2O3 can obviously inhibit the proliferation of the human epidermal carcinoma cells cultured in vitro,and can induce the cells' apoptosis,which may be related to its inhibition effect on the expression of Survivin.
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MTT assay
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Purpose To investigate the effect of arsenic trioxide (As2O3) on Hep-2 cell lines of laryngeal squamous cell carcinoma and provide the experimental basis for the clinical therapy of terminal laryngeal carcinoma. Methods As2O3 at various levels of concentration were used in Hep-2 in vitro. To observe proliferation inhibition, apoptosis and the cell cycle with the growth curve of cell lines, MTT, Wrigh's-Gimesa.DNA agarose gel electrophoresis technique, TUNEL and flow cytometry were used. Results Hep-2 proliferation inhibition was affected by As2O3 and showed the effect of time and dosage. Within a certain time and dosage, apoptotic cells were induced, which depended on As2O3 concentration, Most of the cells were arrested in the G2+M period. Conclusion Arsenic trioxide can induce apoptosis and proliferation inhibition of Hep-2 cell lines of laryngeal squamous cell carcinoma, which can provide a practicable way for the clinical therapy of terminal laryngeal carcinoma.
Arsenic Trioxide
Agarose gel electrophoresis
MTT assay
Growth inhibition
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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.
Arsenic Trioxide
MTT assay
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Objective To decrease the threshold of apoptosis in human nasopharyngeal carcinoma cells in order to explore a new strategy to enhance the sensitivity of chemotherapy by apoptosis-promoting gene bcl-x s. Methods Bcl-x s gene-bearing mammalian expression vector was transfected into CNE-2Z cells. Cells with no transfected bcl-x s gene were taken as controls. After the treatment with arsenic trioxide, IC 50 was calculated using trypan blue exclusion. Apoptotic cells were detected with flow cytometry. Results The IC 50 of cells expressing transfected bcl-x s, treated with arsenic trioxide, significantly decreased compared with that of the controls. The results of flow cytometry analysis showed a significant increase of apoptotic cells in CNE-2Zx s as compared with the controls after treating with the same amount of arsenic trioxide. Conclusion Exogenous bcl-x s expression can enhance the sensitivity of CNE-2Z to arsenic trioxide-induced apoptosis.
Arsenic Trioxide
Trypan blue
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Objective:To study the biological effects of arsenic trioxide (As 2O 3) on human gastric carcinoma cell line SGC-7901 in vitro. Methods:By means of MTT reduction assay, the effect of As 2O 3 on the proliferation of SGC-7901 cells was measured. Morphological changes were observed under the light microscope. Ratio of apoptotic cell was detected by Flow Cytometry and TUNEL. Results:As 2O 3 could significantly inhibit the proliferation of SGC-7901 cells and the inhibitory effect was dose-and-time-dependent. As 2O 3 could also induce a G2/M phase arrest in this cell line. The cells treated with As 2O 3 showed a typical apoptotic morphology and hypodiploid peak before G1 phase. TUNEL detection analysis revealed the DNA fragmentation. Conclusion:As 2O 3 could induce apoptosis of SGC-7901 cells, which could be related to cell cycle arrest.
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Fragmentation
MTT assay
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Objective The current study was designed to investigate the effect of arsenic trioxide(As_(2)O_(3)) on induction of apoptosis in ovarian cancer cell.Methods Cell proliferation was assessed by MTT assays,morphological changes of apoptosis were observed with invert microscope and transmission electron microscope.DNA ladder and cell cycle were examined by DNA agarose gel eletronphores and PI fluorescence flow cytometry(FCM)respectively.Results Under the influence of arsenic trioxide,HO8910 cell exhibited changes of apoptosis both in morphology and in the characteristics of electrophoresis.Meanwhile the cell cycle also showed special change with the apperance of G1 peak and increase of S+G2~M cells.Conclusion Arsenic trioxide inhibits cell proliferation,induces apoptosis in ovarian cancer cell.
Arsenic Trioxide
Agarose gel electrophoresis
MTT 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.
Arsenic Trioxide
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