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Background: Several epidemiological studies have assessed the association of sugary drinks consumption with cancer, but the results remain controversial. Objective: We performed this analysis to evaluate possible causal relationship between sugary drinks consumption and cancer risk and mortality. Methods: We searched PubMed, Embase, and Web of Science databases in English. Observational studies evaluating the association of sugary drinks intake with cancer were included. Random-effects meta-analysis was used to calculate the risk estimates. Results: A total of 71 observational articles with 32 case-control and 39 cohort studies were included in the meta-analysis. 60 addressed cancer risk, and 11 reported cancer mortality. Compared with the lowest level, the highest level of sugar-sweetened beverages (SSB) consumption showed an increased overall cancer risk (RR=1.12 95% CI: 1.06-1.19, P=0.000) and mortality (RR=1.07 95% CI: 1.01-1.14, P=0.029), and fruit juice intake showed a positive association with cancer risk in cohort studies (RR=1.06 95% CI: 1.01-1.11, P=0.013). Subgroup analyses based on cancer type indicated that risk of breast cancer, hepatocellular carcinoma, colorectal cancer, and prostatic cancer mortality had a positive association with SSB consumption. For dose-response analysis, evidence of a linear association was found between overall cancer risk and SSB or fruit juice consumption, and the risk increase by 4% for one servings/d increment in SSB intake and 14% in fruit juice. Conclusions: Our findings suggest the consumption of sugary beverages may increase the risk and mortality of cancer, especially risk of breast cancer, hepatocellular carcinoma, colorectal cancer, and prostatic cancer, and mortality of breast cancer, though the evidence was limited.

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are contributed equally to this work.Abbreviations: ChIP, Chromatin immunoprecipitation; H3K27me3, H3 lysine 27 trimethylation; H3K4me3, H3 lysine 4 trimethylation; HCC, Hepatocellular carcinoma; IGF2, Insulin-like growth factor 2; lncRNAs, Long noncoding RNAs; MANT, the matched adjacent nontumourous tissues; MTT, the methyl thiazolyl tetrazolium; NALT, the normal adult liver tissues;Neg-ctrl, negative control cells; PI, propidium iodide; PRC2, polycomb repressive complex 2; RIP, the RNA immunoprecipitation; sh91H, 91H shRNA; si91H, 91H siRNA; siRBBP5, RBBP5 siRNA; TEPV, tumour embolus of portal vein; TrxG, Trithorax group. AbstractBackground & Aims: Long noncoding RNA 91H is transcribed from the H19/IGF2 locus and contributes to the development of breast and oesophagus cancers by regulating the expression of IGF2, but the regulation mechanism remains poorly characterized. Here, we explored the role of 91H in hepatocellular carcinoma (HCC) and the mechanism of IGF2 expression regulation by 91H.Methods: Firstly, the expression of 91H was analysed in HCC by quantitative RT-PCR, the association of 91H with survival was evaluated by the Kaplan-Meier method and the effect of 91H on the growth and invasion of HCC was investigated by the in vitro and in vivo studies. Then, the association of 91H with the expression of IGF2 was evaluated in HCC tissues, and the effect of 91H on the expression of IGF2 was investigated by 91H knockdown. Finally, the binding of RBBP5 to 91H and the binding of RBBP5, activating H3K4me3 mark and repressive H3K27me3 mark to the P3 and P4 promoters of IGF2 gene were studied by RIP and ChIP respectively. Results:The overexpression of 91H was found in HCC and in association with the growth, metastasis and shorter survival time of HCC. The knockdown of 91H downregulated the IGF2 expression in HCC, and the mechanism was correlated with the decreased enrichment of RBBP5 and H3K4me3 and increased enrichment of H3K27me3 at the bivalent P3 and P4 promoters. Conclusions:The overexpression of 91H promotes tumour growth and metastasis, and is associated with a poor prognosis of HCC at least partially by positively regulating the expression of IGF2 through bivalent histone modification changes characterized by H3K4me3 and H3K27me3 at the P3 and P4 promoters. K E Y W O R D S 91H, bivalent histone modifications, hepatocellular carcinoma, IGF2, Long noncoding RNA | 457 YI et al.

INTRODUCTION: We aimed to assess the effects of 2 isoenergetic intervention diets (a freshwater fish-based diet [F group] or freshwater fish-based and red meat-based diets alternately [F/M group]) on liver steatosis and their relationship with intestinal flora in patients with nonalcoholic fatty liver disease (NAFLD). METHODS:In this open-label, 84-day randomized controlled trial, 34 NAFLD patients with hepatic steatosis ‡10% were randomly assigned to the F group or F/M group in a 1:1 ratio using a computer-generated random number allocation by a researcher not involved in the study. Liver fat content and gut microbiota and its metabolites were measured.