ABSTRACT
Objective To study the radiosensitizing effect of 2'-hydroxyflavanone (2'-HF) on prostate cancer cells,and to preliminarily investigate its mechanism.Methods Colony formation assay,tert-butylhydroperoxide (TBHP) oxidative stress assay,Hoechst staining,and apoptosis flow cytometry using Annexin V-FITC and propidium iodide (PI) were performed to measure the impact of 2'-HF on the radiosensitivity of VCaP prostate cancer cells.Western blot was used to determine the effects of 2'-HF on expression of AKT,phosphorylated AKT (p-AKT),and aldo-keto reductase 1 C3 (AKR1 C3) in VCaP cells and preliminarily investigate the mechanism.Data were analyzed by t test and factorial analysis of variance.Results The results of colony formation assay indicated that after exposure to radiation,VCaP cells treated with 2'-HF had a significantly lower proliferation level than cells in the control group (P=0.010),yielding a sensitization enhancement ratio of 1.19.The resuhs of TBHP oxidative stress assay suggested that VCaP cells treated with 2'-HF had significantly weaker anti-oxidative capacity than cells in the control group (P=0.015).Hoechst staining and apoptosis flow cytometry with Annexin V-FITC and PI indicated that 2'-HF treatment plus irradiation significantly enhanced apoptosis in VCaP cells (P=0.001.The results of Western blot suggested that 2'-HF treatment significantly inhibited the protein expression of p-AKT and AKR1C3 in VCaP cells (P=0.013 and P=0.016).Conclusions 2'-HF can enhance the radiosensitivity of prostate cancer cells,which is probably associated with its inhibitory effects on AKT pathway and AKR1C3 expression in prostate cancer cells.
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Objective To investigate the androgen-like effects of Cordyceps sinensis (CS) and its impact on the radiosensitivity of VCaP prostate cancer cells.Methods The hormone levels and weight index of reproductive organs in mice were determined after gavage with CS.Clonogenic assay was performed to determine the impact of CS on the radiosensitivity of VCaP cells.The 3-(4,5-dimethylthiazol-2-yl)-5 (3-carboxymethonyphenol)-2-(4-sulfophenyl)-2H-tetrazolium assay,flow cytometry,and tumor xenografts in nude mice were performed to determine the effects of CS on the proliferation of VCaP cells (androgen receptor-positive) and PC-3 cells (androgen receptor-negative) in vitro and in vivo.Serum prostate-specific antigen (PSA) levels in nude mice were evaluated.Data were analyzed by one-way analysis of variance or ttest.Results The testosterone level and weight of prostate in mice were significantly higher in the CS group than in the control group ((8.28± 1.94) vs.(2.08± 1.24) ng/ml,P=0.023;(0.53±0.04) vs.(0.31 ± 0.04) mg/g,P =0.006).The radiosensitivity enhancement ratio (ratio of D0 values) was 0.80.The viability of VCaP cells was significantly higher in the CS group than in the control group (1.32 ± 0.07 vs.0.66 ±0.02,P=0.000),and colony forming efficiency was significantly enhanced in the CS group than in the control group (57.0％ ± 1.9％ vs.47.0％ ± 0.6％,P =0.005).VCaP tumor xenografts in nude mice were inclined to grow faster in the CS group than in the control group,and the serum PSA level in the CS group was significantly higher than that in the control group ((0.66 ± 0.04) vs.(0.26 ±0.06) ng/ml,P =0.000).However,CS had no effect on PC-3 cells at the working concentration.Conclusions CS has the androgen-like effects.It may also promote the proliferation and reduce the radiosensitivity of androgen receptor-positive VCaP cells.
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Objective:To study the expression of COX-2 and Survivin in HCC tissues and their relationship for supplying experimental evidence for gene diagnosis and treatment of HCC.Methods:The expression of COX-2 and Survivin was detected in 30 cases of hepatocellular carcinoma and 10 normal liver tissue by Flow cytometry (FCM) and immunohistochemistry (SP).Results:Two experimental methods showed that the positive expression of COX-2 and Survivin in HCC was significanly higher than that in normal liver tissue and there was significanly positive correlation between the expression of COX-2 and Survivin.Conclusion:The hyper-expression of COX-2 and Survivin in tissue can reflex the biological behavior of HCC and there are synergistic effect between them during the development of HCC.A possible mechanism is inhibition of tumor cell apoptosis through upregulating Survivin by COX-2,and promoting abnormal cell proliferation in development of hepatocellular carcinoma.