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The aim of the present study was to explore the effect of esophageal cancer-related gene 2 (ECRG2) protein in combination with cisplatin (DDP) on the proliferation and apoptosis of esophageal cancer cells. A 3-(4, 5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay was used to examine the effects of ECRG2 alone and ECRG2 in combination with DDP on the proliferation of EC9706 esophageal cancer cells. Hoechst 33258 staining was performed to analyze the effects of ECRG2 alone and ECRG2 in combination with DDP on apoptosis in the EC9706 cells. The expression levels of Bcl-2-associated X protein (Bax) mRNA and protein were determined by reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively. The results from the MTT assay revealed that ECRG2 inhibited the proliferation of EC9706 cells and that ECRG2 in combination with DDP had a greater inhibitory effect on cell proliferation. The antiproliferative effects were time- and concentration-dependent, within a certain range of concentrations. The Hoechst 33258 staining results demonstrated that the number of apoptotic cells following treatment with ECRG2 in combination with DDP for 24 h was higher than that following treatment with ECRG2 alone for the same duration. Western blot analysis and RT-PCR results revealed that the expression levels of Bax mRNA and protein were upregulated in cells treated with ECRG2 in combination with DDP compared with those in cells treated with ECRG2 alone. Thus, ECRG2 in combination with DDP had an enhanced inhibitory effect on EC9706 cell proliferation compared with that of ECRG2 alone, and an increased inductive effect on EC9706 cell apoptosis, possibly due to the upregulation of the expression of Bax. [ABSTRACT FROM AUTHOR]

Quercetin is a hydrophobic agent with potential anticancer activity. The aim of the present study was to observe the effects of quercetin on the proliferation of the breast cancer cell line MCF-7 and the gene expression of survivin. The molecular mechanism underlying the antiproliferative effect of quercetin was also investigated. MCF-7 breast cancer cells were treated with various concentrations of quercetin. The inhibitory effect of quercetin on proliferation was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method and the inhibition rate was calculated. Cellular apoptosis was detected by immunocytochemistry and survivin mRNA expression levels were observed using reverse transcription-polymerase chain reaction (RT-PCR). Western blot analysis was used to analyze changes in the expression levels of survivin protein. Quercetin induced the apoptosis of MCF-7 cells and inhibited the proliferation of the MCF-7 breast cancer cells in a time- and concentration-dependent manner. The mRNA and protein expression levels of survivin were reduced as the concentration of quercetin increased. Quercetin inhibited the growth of MCF-7 cells and promoted apoptosis by inducing G0/ G1 phase arrest. It also regulated the expression of survivin mRNA in MCF-7 cells, which may be the mechanism underlying its antitumor effect. [ABSTRACT FROM AUTHOR]

Quercetin is a hydrophobic agent that demonstrates potential anticancer activity. The aim of the present study was to observe the effects of quercetin on the proliferation and apoptosis of the ovarian cancer cell line SKOV-3, and to provide a foundation for the treatment of ovarian cancer using this agent. Ovarian cancer SKOV-3 cells were treated with quercetin at different doses. The inhibitory effect of quercetin on proliferation was detected using the MTT assay and the inhibition rate was calculated. Cell apoptosis was determined using Hoechst staining, and western blot analysis was used to analyze changes in the expression levels of survivin protein. The effects of quercetin on the cell cycle and apoptosis of the SKOV-3 cell line were analyzed using flow cytometry. Quercetin inhibited the proliferation of SKOV-3 cells in a time- and dose-dependent manner. Furthermore, Hoechst staining showed that quercetin induced SKOV-3 cell apoptosis. The protein expression levels of survivin were reduced as the concentration of quercetin increased. Flow cytometric analysis showed that quercetin caused ovarian cancer SKOV-3 cell cycle arrest in the G0/G1 phase and a significant decrease in the percentage of cells at the G2/M phase; furthermore, the apoptosis rate was observed to increase following quercetin treatment. The results in combination indicated that Quercetin could inhibit the proliferation of ovarian cancer SKOV-3 cells, inhibit cell cycle progression from G0/G1 to G2/M and induce cell apoptosis in vitro. [ABSTRACT FROM AUTHOR]