Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.

BackgroundThe results of the studies that have investigated the effects of black tea on blood cholesterol are inconsistent. The aim of this study is to quantitatively assess the effects of black tea on cholesterol concentrations.MethodsPubMed, Embase, MEDLINE, and Cochrane Library (through to July 2014) were searched for randomized controlled trials (RCTs) designed to investigate the effect of black tea on blood cholesterol concentrations. The study quality was assessed by the Jadad scoring criteria. Pooled effect of black tea consumption on blood cholesterol concentrations was evaluated by fixed-effects or random-effects model. Meta-regression analyses were conducted to estimate dose effects of black tea polyphenols on concentrations of blood cholesterol. Subgroup and sensitivity analyses were performed to assess the potential source of heterogeneity.ResultsThe consumption of black tea did not significantly lower TC concentrations either in healthy subjects or patients with coronary artery diseases based on both fixed-effects and random-effects analysis. No significant change was observed in HDL-C concentrations in healthy participants or in subjects with coronary artery disease supplemented with black tea when compared with control participants. The pooled net change of LDL-C in healthy participants was −5.57 mg/dL (95% CI, −9.49 to −1.66 mg/dL; P = 0.005) in fixed-effects analysis and −4.56 (95% CI, −10.30 to 1.17 mg/dL; P = 0.12) in random-effects analysis. No significant net change was observed in LDL-C concentrations in patients with coronary artery disease. Subgroup and sensitivity did not significantly influence the overall outcomes of this meta-analysis. No significant dose effects of black tea polyphenols on blood cholesterol concentrations were detected in meta-regression analyses.ConclusionThe meta-analysis suggests that the consumption of black tea might not have beneficial effects on concentrations of TC, HDL-C, and LDL-C. Further high quality RCTs are needed to definitively draw a causal interpretation of the findings.

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Evidence has demonstrated that Daphnetin has antiangiogenesis activity, indicating it might be a new multi-targeted medication for cancer therapy. Here, we aimed to reveal Daphnetin role in hepatocellular carcinoma (HCC) progression and the underlying mechanism. Huh7 and SK-HEP-1, two human HCC cell lines were used in this study. MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), colony formation, flow cytometry, and tumor-bearing experiments were applied to evaluate the effects of different concentrations of Daphnetin on cell viability, apoptosis, cell cycle, and in vivo tumor formation, respectively. Real-time PCR (Polymerase Chain Reaction)and western blotting were applied to measure the mRNA and protein levels of β-catenin. We observed that Daphnetin inhibited cell viability and tumorigenesis, promoted cell apoptosis, and induced a G1 phase arrest in a dose-dependent manner in both Huh7 and SK-HEP-1 cells, which were rescued by SKL2001, an activator of the Wnt/β-catenin signaling. Taken together, this study reveals that Daphnetin exerts an antitumor role in HCC through the inactivation of Wnt/βcatenin signaling.