The anti-tumor activity of curcumin against androgen-independent prostate cancer cells in vitro and the possible mechanism were investigated. After curcumin treatment, the effect of curcumin on the proliferation of prostate cancer PC-3 cells was assessed by CFSE staining. Flow cytometery (FCM) was performed to analyze the cell cycle and the induction of apoptosis of tumor cells. A luciferase reporter gene assay was used to determine the effects of curcumin on the activities of intracellular NF-κB and AP-1 signaling pathways. The results showed curcumin could effectively inhibit the proliferation of PC-3 cells in vitro (P<0.05). Cells were arrested at G(2)/M phase. After curcumin treatment, the percentage of apoptotic cells was significantly higher than in control group (P<0.05). The results of the luciferase assay revealed that curcumin selectively inhibited the activities of the NF-κB and AP-1 signaling pathways in PC-3 cells significantly. It was suggested that curcumin could exert anti-tumor activity against androgen-independent prostate cancer cells in vitro by inhibiting cellular proliferation and inducing apoptosis, which was probably contributed to the inhibition of transcription factors NF-κB and AP-1.

Immunotherapy which has been in practice for more than 20 years proves effective for the treatment of metastatic renal cell carcinoma (mRCC). Anti-angiogenesis-targeted therapy has recently been identified as a promising therapeutic strategy for mRCC. This study was aimed to evaluate the effectiveness of vascular endothelial growth factor (VEGF) pathway-targeted therapy for mRCC by comparing its effectiveness with that of immunotherapy. The electronic databases were searched. Randomized controlled trials (RCTs) on comparison of VEGF inhibiting drugs (sorafenib, sunitinib and bevacizumab) with interferon (IFN) or placebo for mRCC treatment were included. Data were pooled to meta-analyze. A total of 7 RCTs with 3451 patients were involved. The results showed that anti-VEGF agents improved progression-free survival (PFS) and offered substantial clinical benefits to patients with mRCC. Among them, sunitinib had a higher overall response rate (ORR) than IFN (47% versus 12%, P<0.000001). Bevacizumab plus IFN produced a superior PFS [risk ratio (RR): 0.86, 95% confidence interval (CI): 0.76-0.97; P=0.01] and ORR (RR: 2.19; 95% CI: 1.72-2.78; P<0.00001) in patients with mRCC over IFN, but it yielded an increase by 31% in the risk of serious toxic effects (RR: 1.31; 95% CI: 1.20-1.43; P<0.00001) as compared with IFN. The overall survival (OS) was extended by sorafenib (17.8 months) and sunitinib (26.4 months) as compared with IFN (13 months). It was concluded that compared with IFN therapy, VEGF pathway-targeted therapies improved PFS and achieved significant therapeutic benefits in mRCC. However, the risk to benefit ratio of these agents needs to be further evaluated.

Immunotherapy which has been in practice for more than 20 years proves effective for the treatment of metastatic renal cell carcinoma (mRCC).Anti-angiogenesis-targeted therapy has recently been identified as a promising therapeutic strategy for mRCC.This study was aimed to evaluate the effectiveness of vascular endothelial growth factor (VEGF) pathway-targeted therapy for mRCC by comparing its effectiveness with that of immunotherapy.The electronic databases were searched.Randomized controlled trials (RCTs) on comparison of VEGF inhibiting drugs (sorafenib,sunitinib and bevacizumab) with interferon (IFN) or placebo for mRCC treatment were included.Data were pooled to meta-analyze.A total of 7 RCTs with 3451 patients were involved.The results showed that anti-VEGF agents improved progression-free survival (PFS) and offered substantial clinical benefits to patients with mRCC.Among them,sunitinib had a higher overall response rate (ORR) than IFN (47％ versus 12％,P＜0.000001).Bevacizumab plus IFN produced a superior PFS [risk ratio (RR):0.86,95％ confidence interval (CI):0.76-0.97; P=0.01] and ORR (RR:2.19; 95％ CI:1.72-2.78; P＜0.00001) in patients with mRCC over IFN,but it yielded an increase by 31％ in the risk of serious toxic effects (RR:1.31; 95％ CI:1.20-1.43; P＜0.00001) as compared with IFN.The overall survival (OS) was extended by sorafenib (17.8 months) and sunitinib (26.4 months) as compared with IFN (13 months).It was concluded that compared with IFN therapy,VEGF pathway-targeted therapies improved PFS and achieved significant therapeutic benefits in mRCC.However,the risk to benefit ratio of these agents needs to be further evaluated.

Objective To explore the expression of microRNA(miR)-100-5p in thyroid cancer cells and its regulatory effects on cell proliferation and apoptosis through experiments.Methods The relative expressions of miR-100-5p in thyroid cancer cell lines(TPC-1 and KTC-1)and normal thyroid cell lines(Nthy ori3-1)were detected using fluorescence quantitative PCR.After transfection of miR-100-5p mimic,miR-100-5p inhibitor,and corresponding negative controls(miR-mimic NC,miR-inhibitor NC)into TPC-1 cells,the proliferation condition of TPC-1 cells was detected using CCK-8,and the apoptosis condition of TPC-1 cells was detected using flow cytometry.Prediction and functional enrichment analysis of target genes of miR-100-5p were performed using the miRTarBase and TargetScan7.2 databases.The targeted regulatory effect of miR-100-5p on fibroblast growth factor receptor 3(FGFR3)was validated using Western blot and dual luciferase reporter gene experiments.Results Compared with Nthy-ori3-1 cells,the expression levels of miR-100-5p in TPC-1 cells(1.87±0.03 vs 1.00±0.03)and KTC-1 cells(6.33±0.47 vs 1.00±0.03)were both up-regulated,with significant differences(t=-34.220,-19.588,all P＜0.05).The 450nm absorbance(A450nm)of cells transfected with miR-100-5p mimic at 24,48 and 72 h were higher than the miR-mimic NC group,with significant differences(t=-7.516,-17.828,-8.445,all P＜0.05).Conversely,the A450nm values of cells transfected with miR-100-5p inhibitor at 24,48 and 72 h were lower than the miR-inhibitor NC group,with significant differences(t=6.720,6.782,6.073,all P＜0.05).The apoptosis rate after transfection with miR-100-5p mimic was decreased compared to miR-mimic NC group(7.43％±0.49％vs 10.55％±0.80％),with significant differences(t=5.767,P=0.004).Compared to miR-inhibitor NC group,the apoptosis rate after transfection with miR-100-5p inhibitor was increased(3.19％±0.22％vs 2.64％±0.15％),with significant differences(t=-3.606,P=0.023).Western blot experiments showed that FGFR3 protein expression levels in the miR-100-5p mimic group were down-regulated compared to the miR-mimic NC group(0.78±0.12 vs 1.00±0.00),with significant differences(t=3.071,P=0.037).Compared to the miR-inhibitor NC group,FGFR3 protein expression levels in the miR-100-5p inhibitor group were up-regulated(1.17±0.07 vs 1.00±0.00),with significant differences(t=-4.509,P=0.046).There was no significant difference in the luciferase activity of the FGFR3 wild-type(1.01±0.17 vs 1.00±0.00)and mutant groups(0.99±0.11 vs 1.00±0.00)between miR-100-5p mimic and miR-mimic NC,and the differences were statistically significant(f=-0.057,0.181,P=0.96,0.873).Conclusion MiR-100-5p in thyroid cancer cells was up-regulated,which may promote cell proliferation and inhibit apoptosis.It may become a new biomarker and regulatory target in the diagnosis and treatment of thyroid cancer.

The anti-tumor activity of curcumin against androgen-independent prostate cancer cells in vitro and the possible mechanism were investigated.After curcumin treatment,the effect of curcumin on the proliferation of prostate cancer PC-3 cells was assessed by CFSE staining.Flow cytometery (FCM) was performed to analyze the cell cycle and the induction of apoptosis of tumor cells.A luciferase reporter gene assay was used to determine the effects of curcumin on the activities of intracellular NF-κB and AP-1 signaling pathways.The results showed curcumin could effectively inhibit the proliferation of PC-3 cells in vitro (P＜0.05).Cells were arrested at G2/M phase.After curcumin treatment,the percentage of apoptotic cells was significantly higher than in control group (P＜0.05).The resuits of the luciferase assay revealed that curcumin selectively inhibited the activities of the NF-κB and AP-1 signaling pathways in PC-3 cells significantly.It was suggested that curcumin could exert anti-tumor activity against androgen-independent prostate cancer cells in vitro by inhibiting cellular proliferation and inducing apoptosis,which was probably contributed to the inhibition of transcription factors NF-κB and AP- 1.