Decreased DNA Repair Capacity of UV-Irradiated Cells Following Interferon Treatment
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The aim of this study was to examine the effect of interferons (IFNs) on the recovery of UV-damaged cells by means of measuring cell viability rates. The influence of the recombinant human interferons IFN-α, IFN-βand IFN-γ on the repair capacity of the UV-irradiated human cell lines WISH and HeLa was studied. The ability of cells to repair UV-induced damage was determined by the comet assay and both short- and long-term survival assays in proliferating cell cultures. We found that INFs negatively regulated DNA repair in cells damaged by UV light. One day after treatment, in both cell lines tested, IFN-α had a stronger inhibitory effect than IFN-γ. Combined treatment with different IFNs exhibited a stronger inhibitory effect on cell recovery than treatment with each of them. The protein kinase inhibitor wortmanin further aggravated the effect of IFNs on cell survival.Keywords:
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Objective To investigate the effect of SAHA(suberoylanilide hydroxamic acid)on p53 wild type HeLa cells and p53 knock-down HeLa-E3 cells.Methods The cell's proliferation were determined by MTT after 24,48 and 72 h incubation;the cell cycle distribution and cell death were detected by flow cytometry and typan-blue assay,respectively.Results SAHA significantly suppressed the in vitro proliferation of HeLa and HeLa-E3 cells in a time and dose dependent manner.G2/M arrest and cell death of HeLa cells were also elevated by SAHA in 24 h,while HeLa cells were more sensitive to SAHA than HeLa-E3 cells.Conclusion The results show that the sensitivity of tumor cells to SAHA were influenced by p53.
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Objective To investigate the apoptosis inducing effect of N-4-hydroxyphenyl retinode(4-HPR)and Cisplatin on human HeLa cell lines.Methods MTT assay was employed to examine the growth suppression of the cells.TEM was used to observe the ultrastructural change of HeLa cells treated with 4-HPR and Cisplatin.The apoptosis rate and change in cell cycle of HeLa cells treated with 4-HPR or/and Cisplatin were examined by flow cytometer.Results 4-HPR and Cisplatin both could induce apoptosis of HeLa cells;combined use of 4-HPR and Cisplatin could enhance HeLa cells apoptosis.Conclusion 4-HPR and Cisplatin could induce apoptosis of HeLa cells,and their effect is synergetic.
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Objective:To observe whether the serum pharmacological effect of FL inhibits Hela cell proliferation in cervical cancer.Methods:We used MTT assay to examine the serum pharmacological effect of FL on the decrease im Hela cell,we used TUNEL for quantitive determination of the apoptosis of Hela cell.Results:The FL serum accelerated Hela cell apoptosis..Conclusion:The serum pharmacological effect of FL controls proliferation of Hela cell.which is very important for the gaidance in clinical treatment by the drug.
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Objective To observe the inhibition effect of the extract B of Polygonatum odoratum(EB-PAOA) on human cervix cancer Hela cells.Methods Cervix cancer Hela cells were cultured in vitro and then different concentration of EB-PAOA were added to Hela cells.The growing curve was drawn.MTT assay was adopted to determine the inhibition rate to Hela cells.Results EB-PAOA can inhibit the proliferation of Hela cells,and the inhibition rate is of time and dose dependent.Conclusions EB-PAOA has obvious inhibition effect on Hela cells.
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Objective To explore the effects of iNOS inhibitor 1400 W alone or combined with cisplatin to cervical cancer cell line HeLa. Methods Cervical cancer cell line HeLa was resuscitated and incubated,MTT was used to investigate 1400 W and cisplatin’s effects on HeLa cell growth; flow cytometry was used to detect the HeLa cell apoptosis rate and RT-PCR was used to detecte the E6, p53 mRNA expression of HeLa cell. Results Both cisplatin and 1400 W showed a dose-dependent inhibitory effect on HeLa cell proliferation(P0.05). 1400 W could not increase HeLa cell’s apoptosis, while 1400 W combined cisplatin could both induce apoptosis and decrease E6, p53 mRNA expression of HeLa cell(P0.05). Conclusions 1400 W combined with ciplatin can increase the HeLa cell apoptosis rate than the group cisplatin used alone.Combined with iNOS inhibitor, it can enhance the cisplatin effect on tumor cell. This is possible a promising adjuvant therapy for cervical caner.
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フッ素による培養細胞の増殖抑制機構を検討するため, HeLa細胞ならびにフッ素耐性HeLa細胞 (FR細胞) を用いて実験を行った。耐性細胞は最高2mMのNaFを添加した培地でHeLa細胞を継代し樹立したものである。その結果次の成績が得られた。1. HeLa細胞の増殖は, 0.5mMNaFでわずかに抑制され, 2mMNaFでは全く阻止された。FR細胞は, 2mM NaFでも対照と同じ増殖を示した。2. 2mMNaF存在下でHeLa細胞のタンパク質合成は強く阻害されたが, FR細胞でのタンパク質合成阻害はわずかであった。3. HeLa細胞とFR細胞の細胞質のタンパク質組成をSDS-ポリアクリルアミドゲル電気泳動 (SDS-PAGE) で調べたところ, クーマシーブルー染色で, 両細胞間のペプチドバンドのパターンに明らかな違いは認められなかった。4. HeLa細胞とFR細胞を, 2mM NaF処理した後合成されたタンパク質をSDS-PAGE, オートラジオグラフィーで調べたところ, HeLa細胞では, 分子量約77000ダルトンの強くラベルされる特異的なペプチドが認められた。FR細胞では, NaFの作用をうけないHeLa細胞と同様なペプチドバンドのパターンが見られた。5. この特異的な77000ダルトンのペプチドは, フッ素処理時間の増加と共に強くラベルされる傾向を示した。6. 77000ダルトンのペプチドの細胞内局在は, 形質膜, ミトコンドリア分画, ミクロゾーム分画に認められたが, 核, 可溶性分画には認められなかった。
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Objective To observe the effects of different concentration of TRAIL on cervical cancer HeLa cells.Methods With different concentration of TRAIL role in HeLa cells,the survival fraction of HeLa cells was measured by MTT assay in Chongqing Medical University in 2006.Structures of apoptosis cells were observed by AO/EB fluorescence microscopy.Cell cycle of HeLa cells and apoptosis rates were determined by FACS.Results After treating HeLa cells for 24 h by TRAIL,a good dose-effect relationship was demonstrated by the role of TRAIL in the rate of cell growth inhibition and apoptosis;early and late apoptosis cell can be seen by AO/EB stainning and the hypodiploid peaks were found by FACS checking.The cell cycles were changed.Conclusion The proliferation of HeLa cells can be inhibited and the apoptosis can be induced by TRAIL.
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