Dietary polyphenols and the risk of metabolic syndrome: a systematic review and meta-analysis.

BACKGROUND: Accumulating evidence has suggested that dietary polyphenols may be protective against metabolic syndrome (MetS); however, the available evidence is contradictory. The aim of this meta-analysis was to assess the association between dietary intake of polyphenols and the odds of MetS. METHODS: The PubMed and Scopus databases were systematically searched to obtain eligible studies. The risk of MetS for the highest versus the lowest intakes of total, subclasses and individual polyphenols were examined by pooling odds ratios (OR) and 95% confidence intervals (95%CI) using the random effects model. RESULTS: A total of 14 studies (6 cohort and 8 cross-sectional studies) involving a total of 50,366 participants with 10,879 cases of MetS were included. When various polyphenol compounds were pooled, they were significantly related to a 22% decreased odds of MetS (([5 studies]; OR: 0.78; 95%CI: 0.72-0.85). Higher intakes of total flavonoids (([9 studies]; OR: 0.78; 95%CI: 0.72-0.85), flavan-3-ols (([2 studies]; OR: 0.64; 95%CI: 0.43-0.94), isoflavones (([3 studies]; OR: 0.84; 95%CI: 0.75-0.93), stilbenes (([4 studies]; OR: 0.86; 95%CI: 0.76-0.97), flavones (([2 studies]; OR: 0.79; 95%CI: 0.71-0.89), and quercetin (([2 studies]; OR: 0.63; 95%CI: 0.43-0.93) were also significantly associated with a decreased risk of MetS. The associations were not modified by the age of the participants. No association was found for total polyphenols, phenolic acids, lignans, anthocyanins, and flavonols. CONCLUSION: The results of this meta-analysis supported that higher polyphenol intake can lower the risk of MetS.

ETS transcription factor ELK3 in human cancers: An emerging therapeutic target.

Cancer is a genetic and complex disorder, resulting from several events associated with onset, development, and metastasis. Tumor suppressors and oncogenes are among the main regulators of tumor progression, contributing to various cancer-related behaviors like cell proliferation, invasion, migration, epithelial-mesenchymal transition (EMT), cell cycle, and apoptosis. Transcription factors (TFs) could act as tumor suppressors or oncogenes in cancer progression. E-twenty-six/E26 (ETS) family of TFs have a winged helix-turn-helix (HLH) motif, which interacted with specific DNA regions with high levels of purines and GGA core. ETS proteins act as transcriptional repressors or activators to modulate the expression of target genes. ETS transcription factor ELK3 (ELK3), as a type of ETS protein, was shown to enhance in various cancers, suggesting that it may have an oncogenic role. These studies indicated that ELK3 promoted invasion, migration, cell cycle, proliferation, and EMT, and suppressed cell apoptosis. In addition, these studies demonstrated that ELK3 could be a promising diagnostic and prognostic biomarker in human cancer. Moreover, accumulating data proved that ELK3 could be a novel chemoresistance mediator in human cancer. Here, we aimed to explore the overall change of ELK3 and its underlying molecular mechanism in human cancers. Moreover, we aimed to investigate the potential role of ELK3 as a prognostic and diagnostic biomarker as well as its capability as a chemoresistance mediator in cancer.