Abstract. Soy isoflavones are compounds found in soybean and soybean products. They have been reported to possess numerous physiological properties, such as antitumor, antimenopausal (female) osteoporosis and anti-aging. They have also been reported to improve learning and memory skills in menopausal women and aid in the prevention and treatment of heart disease, diabetes and Kawasaki disease (KD). In this review, the effects of soy isoflavones on various diseases were analyzed. Based on the analysis, it was hypothesized that the function of soybean isoflavones in the prevention and treatment of various diseases results from their phytoestrogen and antioxidant properties. However, due to their phytoestrogen properties, it is recommended that the risks of soy isoflavone intake as food and̸or medical treatment be further evaluated.

BackgroundSeveral studies have focused on the association between the lipid-lowering efficacy of statins and the SLCO1B1 c.521T>C polymorphism; however, the results are conflicting. The effects of statins show significant variability between individuals. This meta-analysis aimed to investigate the effects of the SLCO1B1 c.521T>C polymorphism on the lipid-lowering effects of statins.MethodsWe systematically searched PubMed and Web of Science to screen relevant studies. Meta-analysis was performed to identify the association between SLCO1B1 c.521 polymorphisms and the lipid-lowering effects of statinson the basis of the standard mean difference (SMD) and 95% confidence intervals (CIs). Additionally, we checked for heterogeneity (I2) among studies and evidence of publication bias. We obtained eight studies including 2,012 wild genotype (T/T) and 526 variant genotype (T/C and C/C) cases.ResultsNo significant difference was observed in the lipid-lowering efficacy of statins between the wildand variant genotypes of SLCO1B1, with a pooled SMD of 0.03 (95% CI: -0.07-0.13). Furthermore, there was no significant effect in the meta-analyses of the variant heterozygote, homozygote, and Chinese populations. Subgroup meta-analysis indicated that the timerequired for the statin to take effectdid notsignificantly affect the association between lipid-lowering efficacy of statins and SLCO1B1 c.521T>C polymorphism. However, thewild genotype improved the lipid-lowering efficacy of simvastatin with a pooled SMD of -0.26 (95% CI: -0.47- -0.05).ConclusionsNo significant association was detected between the lipid-lowering efficacy of statins and the SLCO1B1 c.521T>C polymorphism, with the exception of simvastatin.

Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-inducible factor-1 (HIF-1α) and interleukin-6 (IL-6), which initiate the TME formation. HIF-1α and IL-6 promote regulatory T cells (Tregs) proliferation and migration through the MAPK/CDK4/6/Rb and STAT3/SIAH2/P27 signaling pathways, respectively. IL-6 also promotes the production of HIF-1α and enhances the self-regulation of Tregs in the process of tumor microenvironment (TME) formation. In this review, we discuss how the crosstalk between the CARMA1–BCL10–MALT1 signalosome complex (CBM complex)/NF-κB and MAPK/P27 signaling pathways contributes to the formation of the TME, which may provide evidence for potential therapeutic targets in the treatment of solid tumors.

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Background: Programmed cell death protein 1 (PD-1), as an immune checkpoint cell membrane receptor, negatively regulates T cell activation via its immune receptor, the tyrosine-based switch motif (ITSM). The purpose of this research was to evaluate the antitumor activity T cells with the ITSM mutation of PD-1 on non-small cell lung cancer (NSCLC) in vitro and in vivo.Methods: In this study, the tyrosine of ITSM in cytotoxic T cells was mutated using the adenine base editor (ABE)-xCas9 system to evaluate its effect on the antitumor activity of T cells against NSCLC. Results: Results showed that the PD-1-deficient T cells enhanced the death of the cocultured NSCLC cells compared with the normal T cells and saline solution. PD-1-deficient T cells also changed the interleukin 2(IL-2), interferon γ (IFN-γ), tumor necrosis factor α (TNF-α), and granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion of T cells compared with those of the normal T cells. The effectiveness of ITSM mutation in enhancing the antitumor activity of PD-1-deficient T cells was verified in vivo by using a mouse xenograft model. The xenografted mice treated with PD-1-deficient T cells demonstrated repressed tumor growth of the NSCLC cells compared with those treated with normal T cells and saline solution. Conclusions: The mutation of ITSM in cytotoxic T cell via the ABE-xCas9 system can significantly enhance the antitumor activity of T cells.