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Objective To investigate the diagnostic value of prostate specific antigen density (PSAD),Gleason score and serum ferritin (SF) in bone metastases from prostate cancer.Methods 45 patients diagnosed with bone metastases from prostate cancer in our hospital from January 2015 to October 2017 were selected as metastasis group.90 cases without bone metastases in prostate cancer were selected as control group.The PSAD,SF and Gleason scores of the two groups were measured and compared.Receiver operating characteristic (ROC) curve was used to analyze the three indexes to predict the clinical value of bone metastases in patients with prostate cancer.Results The serum PSA,SF,prostate volume,PSAD levels in metastasis group were significantly higher than those in the control group,with statistically significant difference (P ＜ 0.05);the average Gleason scores metastasis group were significantly higher than the control group (P ＜ 0.05);The sensitivity and specificity of SF combined with PSAD and Gleason score diagnosis in patients with prostate cancer bone metastasis was 95.64％ and 91.30％ respectively,the area under the curve (AUC) value is 0.930.Conclusions Detection and analysis of PSAD,SF,and Gleason scores in patients with prostate cancer will help to evaluate whether or not the patients have bone metastases.
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Objective To detect the treatment effect of PC3 cells with triptolide on altering the expression of genes.Methods MTT assay was used to detec the inhibition of proliferation.Apoptosis was detected by Annexin-V/PI staining.RT-PCR was used to analyze the mRNA expressions of BCL-2,BAX,PIG3,P21,FAS,CASPASE3.Results Triptolide caused a time - and dose - dependent inhibition of cell proliferation,and IC50 of 24 h and 48 h were 18.3 ng/ml and 13.5 ng/ml,respectively.Compared with the 24 h group,the low concentration of triptolide(5 ng/ml,t =1.47,P ＞0.05)and the high concentration of triptolide ( 160 ng/ml,t =0.91,P ＞0.05)had no statistical significance in 48 h group,while 10 ng/ml( t =3.26,P ＜0.05),20 ng/ml( t =4.21,P ＜0.05),40 ng/ml( t =4.09,P ＜0.05),80 ng/ml( t =2.91,P ＜ 0.05 )had statistical significance.At the concentration of 18.3 ng/ml,triptolide induced PC3 cells apoptosis in a time - dependent manner.Compared with the control group,Anexin-V( + )/PI(-)was(5.42±2.21)％(t =3.52,P ＜0.05)in 6h,(13.51±3.37)％(t =6.53,P ＜0.01) 12h,(29.3 ±4.53)％ ( t =8.74,P ＜0.01) 24 h group separately,and it had statistical significance.RTPCR showed that 18.3 ng/ml triptolide up-regulated the mRNA expression of BAX and PIG3,down-regulated P21 and BCL-2.FAS and CASPASE3 did not show obvious changes.Conclusions Triptolide inhibits the proliferation of PC3 and induces apoptosis,and the changes of BCL-2,BAX,PIG3 and P21 may play an important role in the apoptosis of PC-3 cells.
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Objective To observe the effects of ( - )-epigallocatechin-3-gallate (EGCG) on human prostate cancer xenografted tumor growth and connexin43 expression in nude mice,and explore the mechanism of the EGCG on prevention for prostate cancer.Methods The methyl thiazolyl tetrazolium and annexin-V/PI double-labeled flow cytometry methods were used to observe the growth inhibiting rate (IR)and apoptosis rate (AR) of human prostate cancer cell line PC-3 which was treated by EGCG at different concentration (10,20 and 40 mg/L,respectively).The scrape-loading fluorescence dye transfer method was applied to assess the gap junction intercellular communication (GJIC) through fluorescence microscope.PC-3 cells were subcutaneously transplanted to establish tumor-bearing nude mice model.A total of 32 mice were randomly divided into four groups,both control group and three treatment groups were treated with different doses of EGCG ( 10,20 and 40 mg/kg,respectively).After two weeks,the mice prostate tumor tissues were taken out.The tumor wet weight was measured and tumor growth inhibiting rate was calculated.The tumor microvascular density (MVD) and apoptosis index (AI) were detected by the immunohistochemical techniques and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling techniques,respectively.Semi-quantitative reverse transcription polymerase chain reaction was used to examine the expression level of the Cx43 mRNA.Results EGCG at concentration ( 10 and 20 mg/L) could significantly inhibit the proliferation[(22.33 ±4.62)％,(38.67 ±5.67)％ vs (3.47 ±0.31 )％,P ＜0.01],induce the apoptosis [(7.84 ± 1.37 ) ％,( 24.53 ± 2.28 ) ％ vs ( 2.17 ± 0.70 ) ％,P ＜ 0.01] and enhance the GJIC of PC-3 cells.EGCG of different doses could inhibit prostate cancer xenografted tumor growth,induce tumor cells apoptosis and inhibit angiogenesis.EGCG ( 20 and 40 mg/kg) could effectively up-regulate Cx43 mRNA expression in xenografted tumor (0.58 ± 0.08,0.80 ± 0.07 vs 0.42 ± 0.04,P ＜ 0.0 ).The effects had significant correlation with the dose-dependent of EGCG ( P ＜ 0.05 ).Conclusions EGCG could up-regulate the Cx43 expression and enhance the gap junction intercellular communication mediated by Cx43 in the prostate tumor,which provide the experimental evidence for the mechanism of its effectively inhibiting the prostate cancer growth.
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The clinical and pathological materials of 83 cases of prostatic carcinoma (PC) were reviewed retrospectively and the tissue specimens of PC were marked with prostate-specific antigen (PSA). According to the criteria of Dhom's classification of prostatic carcinoma. 66 cases out of the 83 (79. 5%) were of the common variety of PC, 14 cases (10. 9%) were of the rare variety and 3 cases (3. 6%) could not be classified with Dhom's method. Among the 66 cases of common prostatic carcinoma, 41 cases (49. 4%) exhibited a pathological structure of u-riiforrn pattern and 25 cases (30. 1%) of pluriform pattern. Well-differentiated adenocarcinoma, cribriform carcinoma and carcinoid of the prostate were strongly positive to PSA marking; poorly-differentiated adenocarcinoma and almost all the prostatic carcinomas of the rare variety and with the structure of pluriform pattern were positive or weakly positive; undifferentiated solid carcinoma and small cell carcinoma were very weakly positive; and squamous cell carcinoma was negative. In addition, other methods for the pathological classification of prostatic carcinoma used currently at home and abroad were compared and discussed.