Study on Arsenic Trioxide Induced Apoptosis of Human Gastric Carcinoma Cell Line SGC-7901 in Vitro
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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.Keywords:
Arsenic Trioxide
Fragmentation
MTT assay
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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
Fragmentation
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Objective To study the biological effects of arsenic trioxide(As_2O_3) on human gastric cancer cells MKN-28 in vitro.Methods By means of light microscope,MTT reduction assay and flow cytometry to observe apoptosis of human gastric cancer cells in different effect time and concentration of As_2O_3.Results As_2O_3 could significantly inhibit the proliferation of MKN-28 cells and the inhibitory effect was dose-and-timed ependent.The cells treated by As_2O_3 showed a typical apoptotic morphology and hypodiploid peak before G_1 phase.Conclusion As_2O_3 not only could inhibit significantly the proliferation of MKN-28 cells but also could induce apoptosis of MKN-28 cells.
Arsenic Trioxide
Gastric carcinoma
MTT assay
Growth inhibition
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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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To explore the potential therapeutic effect of arsenic trioxide(As₂O₃ ) on human lung cancer.Cell growth curves, cell proliferation, cell cycle and apoptosis of human lung cancer cell line GLC-82 were detected by theMTT method and flowcytometry (FCM) .The data showed that As₂O₃ significantly inhibited proliferation of GLC-82 cells and the inhibiting effects had a dose-and time-dependence. The cell proliferation inhibition rate was 81. 05% when treated with 4. 0 Lmol/L As₂O₃ for 96 hours. The change of DNA content of GLC-82 cells indicated that As₂O₃ was able to block cell cycle progress in G2/M phase, with appearance of sub-G1 peak in a dose-dependent manner.As₂O₃ can effectively inhibit the proliferation of human lung cancer cell line GLC-82 and the possible mechanisms may be related to G2/M phase arrest and apoptosis induced by As₂O₃.
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AIM To study the effects of arsenic trioxide and HCPT on different degrees of differentiated gastric cancer cells(SGC-7901,MKN-45,MKN-28)with respect to both cytotoxicity and induction of apoptosis in vitro. METHODS The cytotoxicity of As_2O_3 and HCPT on gastric cancer cells was determined by MTT assay.Morphologic changes of apoptosis of gastric cancer cells were observed by light microscopy and transmission electron microscopy. Apoptosis and cell cycle changes of gastric cancer cells induced by HCPT and As_2O_3 were investigated by TUNEL method and flow cytometry. RESULTS As_2O_3 and HCPT had remarkable cytotoxic effects on different degrees of differentiated gastric cancer cells.The IC_(50)of As_2O_3 on well differentiated gastric cancer cell MKN-28,moderately differentiated gastric cancer cell SGC-7901,and poorly differentiated gastric cancer cell MKN-28 were 8.91 μmol/L,10.57 μmol/L,and 11.65 μmol/L,respectively.The IC_(50) of HCPT on MKN-28,SGC-7901,and MKN-45 were 9.35 mg/L,10.21 mg/L,and 12.63 mg/L respectively after 48 h treatment.After 12 h of exposure to both drugs,gastric cancer cells exhibited morphologic features of apoptosis, including cell shrinkage,nuclear condensation, and formation of apoptotic bodies.A typical subdiploid peak before G_0/G_1 phase was observed by flow cytometry.The apoptotic rates of SGC- 7901,MKN-45,and MKN-28 were 13.84%, 22.52%,and 9.68%,respectively after 48 h exposure to 10 μmol/L As_2O_3.The apoptotic rates of SGC-7901,MKN-45,and MKN-28 were 21.88%, 12.35%,and 30.26%,respectively after 48 h exposure to 10 mg/L HCPT.The apoptotic indice were 7%-15% as assessed by TUNEL method. The effect of As_2O_3 on SGC-7901 showed remarkable cell cycle specificity,which induced cell death in G_1 phase,and blocked G_2/M phase. HCPT also showed a remarkable cell cycle specificity,by inducing cell death and apoptosis in G_1 phase and arrest of proliferation at S phase. CONCLUSION As_2O_3 and HCPT exhibit significant cytotoxicity on gastric cancer cells by induction of apoptosis.As_2O_3 and HCPT might have a promising prospect in the treatment of gastric cancer,which needs to be further studied.
Arsenic Trioxide
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 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.
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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 effect of arsenic trioxide(As2O3)on the cell proliferation,cell cycle,and cell apoptosis in colorectal can-cer cell line HT-29.Methods: The cell proliferation and the cell cycle and apoptosis of HT-29 cells were determined by MTT assay and flow cytometry,respectively.The morphological changes of HT-29 cells were observed under light microscope.Results: As2O3 inhibited the prolife-ration of HT-29 cells in a dose-and time-dependent manner,and the 50% inhibitory concentrations(IC50)were 40.03,13.76,and 4.53 μmol/L 24,48,and 72 hours after the administration of As2O3,respectively.G2/M phase arrest and cell apoptosis were induced by As2O3,and sub-G0G1 phase cells increased with the decrease of G2/M phase cells 24 hours after the administration of As2O3.The number of mitotic and apoptotic cells increased 12 to 72 hours after the administration of 0.5 to 5 μmol/L of As2O3.Conclusion: As2O3 could inhibit the prolifera-tion of colorectal cancer cell line HT-29 and induce G2/M phase arrest and cell apoptosis.
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This study was aimed to investigate the apoptosis induced by arsenic trioxide (As2O3) in lymphoma Raji cells and its possible mechanisms. The inhibitory effect of different concentration of As2O3 on cell proliferation was tested by MTT assay. Apoptosis was observed with electron microscope and DNA electrophoresis. The distribution of cell cycles and cell apoptosis were detected by flow cytometry. The results showed that the 1-8 micromol/L As2O3 inhibited Raji cell growth effectively in a dose-and time-dependent manner. As2O3 at 2-8 micromol/L could induce the cell apoptosis and cell cycle arrest. However, As2O3 at 1 micromol/L inhibited Raji cells proliferation only by cell cycle arrest, without any signs of cell apoptosis. In conclusion, substantial proliferation inhibition, cell cycle arrest and apoptosis in Raji cells could be induced by As2O3. Cell cycle arrest happens with apoptosis, when treated with As2O3.
Raji cell
Arsenic Trioxide
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