AimsTo evaluate current status of prostate cancer incidence and mortality worldwide, and compare the global trends of incidence and mortality in the past two decades and in the most recent period.MethodsData on the incidence and mortality of prostate cancer for 174 countries in 2020 were obtained from the GLOBOCAN 2020 database, and associations with the human development index (HDI) were evaluated. Data for trend analyses in 89 countries from 2000 to 2019 were retrieved from the Global Burden of Disease 2019 platform. Age standardized incidence rate (ASIR) and mortality rate (ASMR) were calculated by using the Segi's population. The average annual percent changes (AAPC) of ASIRs and ASMRs were evaluated by joinpoint regression analysis.ResultsA total of 1 414 259 new cases of prostate cancer and 375 304 related deaths were reported in 2020 globally. HDI was positively correlated with ASIRs (P < 0.001) and negatively correlated with ASMRs (P < 0.001). In the past two decades, ASIRs have been increasing in 65 countries, stable in 15 countries and decreasing in 9 countries, and ASMRs have been increasing in 19 countries, stable in 25 countries and decreasing in 45 countries, respectively. In the most recent period, 44 countries have increasing ASIRs, and 32 countries have decreasing ASMRs, respectively. For instance, in the United States of America, the AAPC of ASIRs significantly decreased by 0.62% and ASMRs significantly decreased by 1.22% from 2000 to 2019, while the AAPC from 2015 to 2019 significantly increased by 0.49% for ASIRs and significantly increased by 0.48% for ASMRs.ConclusionThe magnitude of increasing incidence and decreasing mortality of prostate cancer is attenuated in the recent period. Further study is needed to analyze the absolute effect of risk factors, PSA screening and treatment.

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BackgroundThe aim of this study was to investigate the effects of Atractylenolide-I (AT-I), a naturally occurring sesquiterpene lactone isolated from Atractylodes macrocephala Koidz, on human ovarian cancer cells.Material/MethodsThe viability and anchorage-independent growth of ovarian cancer cells were evaluated using MTT and colony formation assay, respectively. Cell cycle and apoptosis were detected with flow cytometry analysis. The level of cyclin B1 and CDK1 was measured using qPCR and ELISA analysis. The expression of Bax, cleaved caspase-9, cleaved caspase-3, cytochrome c, AIF, and Bcl-2, and phosphorylation level of PI3K, AKT, and mTOR were determined with Western blot analysis.ResultsAT-I decreased the cell viability and suppressed anchorage-independent growth of A2780 cells. Cell cycle was arrested in G2/M phase transition by AT-I treatment, which was related to decreased expression of cyclin B1 and CDK1 in a dose-dependent manner. In addition, the treatment induced apoptosis, as shown by up-regulation of Bax, cleaved caspase-9, cleaved caspase-3, and cytosolic release of cytochrome c and AIF, and down-regulation of Bcl-2, in a dose-dependent manner. Then, the effects of AT-I on PI3K/Akt/mTOR pathways were examined to further investigate the underlying anti-cancer mechanism of AT-I, and the results showed that treatment with AT-I significantly decreased the phosphorylation level of PI3K, Akt, and mTOR.ConclusionsThis study demonstrated that AT-I induced cell cycle arrest and apoptosis through inhibition of PI3K/Akt/mTOR pathway in ovarian cancer cells. These results suggest that AT-I might be a potential therapeutic agent in the treatment of ovarian cancer.

Growing evidence has suggested a possible relationship between dietary calcium intake and metabolic syndrome (MetS) risk. However, the findings of these observational studies are inconclusive, and the dose-response association between calcium intake and risk of MetS remains to be determined. Here, we identified relevant studies by searching PubMed and Web of Science databases up to December 2018, and selected observational studies reporting relative risk (RR) with 95% confidence interval (CI) for MetS based on calcium intake and estimated the summary RRs using random-effects models. Eight cross-sectional and two prospective cohort studies totaling 63,017 participants with 14,906 MetS cases were identified. A significantly reduced risk of MetS was associated with the highest levels of dietary calcium intake (RR: 0.89; 95% CI: 0.80–0.99; I2 = 75.3%), with stronger association and less heterogeneity among women (RR: 0.74, 95% CI: 0.66–0.83; I2 = 0.0%) than among men (RR: 1.06, 95% CI: 0.82–1.37; I2 = 72.6%). Our dose-response analysis revealed that for each 300 mg/day increase in calcium intake, the risk of MetS decreased by 7% (RR: 0.93; 95% CI: 0.87–0.99; I2 = 77.7%). In conclusion, our findings suggest that dietary calcium intake may be inversely associated with the risk of MetS. These findings may have important public health implications with respect to preventing the disease. Further studies, in particular longitudinal cohort studies and randomized clinical trials, will be necessary to determine whether calcium supplementation is effective to prevent MetS.