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AIM:To investigate the effect of all-trans retinoic acid ( ATRA) on the viability of gastric cancer cell SGC-7901 and the sensitivity to radiotherapy .METHODS:MTT assay was used to examine the cell viability .Radio-sensitivity and cell cycle were determined by colony formation assay and flow cytometry , respectively .The mRNA levels of Bax, Bcl-2, survivin and NF-κB in the cells were measured by RT-qPCR.RESULTS: ATRA inhibited the viability of SGC-7901 cells in a concentration-dependent manner .The maximal inhibition was at concentration of 8 μmol/L.Colony formation assay revealed that the combination of ATRA with X-ray treatment significantly reduced the values of D 0 and Dq, and shifted down the fitting survival curve , as compared with radiotherapy alone .Moreover , ATAR markedly decreased the percentage of G2/M phase in the SGC-7901 cells (P<0.05).In addition, following ATRA treatment, the mRNA levels of Bcl-2 and survivin were decreased (P<0.05), whereas the mRNA levels of Bax and NF-κB were increased (P<0.05). CONCLUSION:ATRA enhances the sensitivity of SGC-7901 cells to radiotherapy , inhibits G2/M arrest and regulates the mRNA expression of Bax , Bcl-2, survivin and NF-κB.
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Objective To explore mechnism and effect of fentanyl on proliferation of gastric cancer SGC-7901 cell.Methods Gastric cancer SGC-7901 cell was cultured with fentanyl of 0 (negative control), 0.5, 5 and 50 nmol/L, MTT method was used to detect the effect of fentanyl on SGC-7901 viability.The effect of fentanyl on SGC-7901 cell cycle was measured by flow cytometry.The level of cell related protein,cell cycle protein cyclin D1, Bcl-2.Results Compared with control group, fentanyl (0.5, 5, 50 nmol/L) could inhibit SGC-7901 cell viability, and the inhibitory rate was highest at 48 h.0.5, 5, 50 nmol/L fentanyl made cell cycle arrested in G1 phase.Compared with control group, fentanyl can significantly inhibit cyclinD1 and Bcl-2 expression with drug concentration increasing(P<0.05).Conclusion These results suggeste fentanyl inhibit proliferation of gastric cancer SGC-7901 cell.
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Objective To explore effect of isoorientin on gastric cancer cell autophagy.Methods Isoorientin and autophagy activator and effect of inhibitors on proliferation of human gastric cancer cell line SGC-7901 by MTT assay.Cell apoptosis was detected by flow cytometry.Production of autophagy lysosomal in gastric cancer SGC-7901 cells was obseroved by AO and MDC staining.Characteristic expression of autophagy protein was analysed by Western blot.Results MTT assay indicated that isoorientin could inhibit gastric cancer cell growth, RAP has the same effects, but 3-MA inhibition of apoptosis.Flow cytometry was used to detect the apoptosis rate of isoorientin and RAP could promote cell apoptosis , while 3-MA had the opposite effect.In AO staining, the red light appeared in the cells, and the green fluorescence appeared in the cells of MDC staining, which showed that there was an autophagy in the cells.Western blot test found the isoorientin was cell autophagy specific protein LC-3II, Beclin-1 expression increased, 3-MA suppressed the expression of the two proteins, and RAP had the opposite effect.Conclusion Isoorientin could induce apoptosis in gastric cancer SGC-7901 cells, autophagy is involved in the process of death.
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Objetive: To study the effect of soybean isoflavone(SI) on the growth of gastric cancer cell SGC-7901 during hypoxia and its mechanisms. Method: The environment of hypoxia was established by GasPaK method. The effect of SI was determined by MTT and FCM which was used for studying apoptosis and cell cycle of SGC-7901. Electron microscopy was used to study the effects of SI on apoptosis and necrosis of SGC-7901. Cell-immunochemistry was used to observe the change of hypoxia-inducible factor HIF-1? and FAS expression. Results: SI could inhibit significantly the growth of SGC-7901, and arrest the cell in G2/M phases during normal and hypoxia environment. The inhibitory effect was elevated significantly during hypoxia. Electron microscopy showed the cell apoptosis and necrosis. FAS expression was elevated by SI during normal and hypoxia environment, and HIF-1? expression was downregulated during hypoxia. Conclusion: SI can inhibit SGC-7901 cell growth via arrest of cell cycle, elevated expression of FAS, apoptosis and necrosis induction and other pathways. The inhibition of the increased HIF-1? expression is probably the mechanism of the inhibitory effects of SI during hypoxia.
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Objective:To study the inhibitory effects of soybean isoflavones and its induction of apoptosis of human gastric cancer cell SGC-7901.Methods:MTT,FCM and electron microscope were used to study the effects of soybean isoflavones on SGC-7901.Results:MTT showed that the soybean isoflavones inhibited SGC-7901 growth.It could arrest the cell in G2/M,electron microscope showed soybean isoflavones could reduce apoptosis.Conclusion:Soybean isoflavones inhibits SGC-7901 cells growth via apoptosis reduction.