Zn metal has been regarded as the most promising anode for aqueous batteries due to its high capacity, low cost, and environmental benignity. Zn anode still suffers, however, from low Coulombic efficiency due to the side reactions and dendrite growth in slightly acidic electrolyte. Here, the Zn plating/stripping mechanism is thoroughly investigated in 1 M ZnSO 4 electrolyte, demonstrating that the poor performance of Zn metal in mild electrolyte should be ascribed to the formation of a porous by-product (Zn 4 SO 4 (OH) 6 •xH 2 O) layer and serious dendrite growth. To suppress the side reactions and dendrite growth, a highly viscoelastic polyvinyl butyral (PVB) film, functioning as an artificial solid/electrolyte interphase (SEI), is homogeneously deposited on the Zn surface via a simple spin-coating This article is protected by copyright. All rights reserved.2 strategy. This dense artificial SEI film not only effectively blocks water from the Zn surface but also guides the uniform stripping/plating of Zn ions underneath the film due to its good adhesion, hydrophilicity, ionic conductivity, and mechanical strength. Consequently, this side-reaction-free and dendrite-free Zn electrode exhibits high cycling stability and enhanced Coulombic efficiency, which also contributes to enhancement of the full-cell performance when it is coupled with MnO 2 and LiFePO 4 cathodes.

BackgroundHigh frequency of recurrence is the major cause of the poor outcomes for patients with hepatocellular carcinoma (HCC). microRNA (miR)-182-5p emerged as a high-priority miRNA in HCC and was found to be related to HCC metastasis. Whether the expression of miR-182-5p in tumor tissue correlated with early recurrence in HCC patients underwent curative surgery was unknown.MethodsReal-time PCR (RT-PCR) and in situ hybridization (ISH) were conducted to assess the expression of miR-182-5p in HCC cells and tissues. Cell Counting Kit-8 (CCK-8), transwell assays were performed to detected cells proliferation and migration ability. Flow cytometry assays were used to detect cell apoptosis rate, and xenograft model was employed to study miR-182-5p in HCC growth and lung metastasis. The target of miR-182-5p was validated with a dual-luciferase reporter assay and western blotting. Immunohistochemistry, immumoblotting, and immunoprecipitation were performed to test relative protein expression.ResultsWe showed that high expression of miR-182-5p in tumor tissues correlated with poor prognosis as well as early recurrence in HCC patients underwent curative surgery. miR-182-5p enhanced motility and invasive ability of HCC cells both in vitro and in vivo. miR-182-5p directly targets 3′-UTR of FOXO3a and repressed FOXO3a expression, activating AKT/FOXO3a pathway to promote HCC proliferation. Notably, miR-182-5p activated Wnt/β-catenin signaling by inhibiting the degradation of β-catenin and enhancing the interaction between β-catenin and TCF4 which was mediated by repressed FOXO3a.ConclusionsConsistently, miR-182-5p can be a potential predictor of early recurrence for HCC patients underwent curative surgery, and FOXO3a plays a key mediator in miR-182-5p induced HCC progression.

S100A8/A9 proteins are members of EF-hand calcium-binding proteins secreted by neutrophils and activated monocytes. S100A8/A9 has cell growth-promoting activity at low concentrations by binding to the receptor for advanced glycation end products (RAGE). In this study, we report for the first time that S100A8/A9 promoted the invasion of breast cancer cells depending on RAGE. In addition, RAGE binding to S100A8/A9 promoted the phosphorylation of LIN-11, Isl1, and MEC-3 protein domain kinase, as well as cofilin. This phosphorylation is a critical step in cofilin recycling and actin polymerization. Interestingly, RAGE binding to S100A8/A9 enhanced cell mesenchymal properties and induced epithelial-mesenchymal transition. Mechanistically, RAGE binding to S100A8/A9 stabilized Snail through the NF-κB signaling pathway. Based on these observations, RAGE expression in breast cancer cells was associated with lymph node and distant metastases in patients with invasive ductal carcinoma. Moreover, RAGE binding to S100A8/A9 promoted lung metastasis in vivo. In summary, our in vitro and in vivo results indicated that RAGE binding to S100A8/A9 played an important role in breast cancer invasion/metastasis. This study identified both RAGE and S100A8/A9 as potential anti-invasion targets for therapeutic intervention in breast cancer.

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Integrin β4 (ITGB4) is a transmembrane receptor involved in tumorigenesis and the invasiveness of many cancers. However, its role in hepatocellular carcinoma (HCC), one of the most prevalent human cancers worldwide, remains unclear. Here, we examined the involvement of ITGB4 in HCC and explored the underlying mechanisms. Real-time PCR and immunohistochemical analyses of tissues from 82 patients with HCC and four HCC cell lines showed higher ITGB4 levels in tumor than in adjacent non-tumor tissues and in HCC than in normal hepatic cells. Silencing of ITGB4 repressed cell proliferation, colony forming ability and cell invasiveness, whereas ectopic expression of ITGB4 promoted the proliferation and invasion of HCC cells and induced epithelial to mesenchymal transition (EMT) in parallel with the upregulation of Slug, as shown by transwell assays, WB and immunocytochemistry. Knockdown of Slug reduced cell viability inhibited invasion and reversed the effects of ITBG4 overexpression on promoting EMT, and AKT/Sox2-Nanog may also be involved. In a xenograft tumor model induced by injection of ITGB4-overexpressing cells into nude mice, ITGB4 promoted tumor growth and metastasis to the lungs. Taken together, our results indicate that ITGB4 plays a tumorigenic and pro-metastatic role mediated by Slug and suggest IGTB4 could be a prognostic indicator or a therapeutic target in patients with HCC.

Bmal1 is a transcription factor that plays a central role in the regulation of circadian rhythms. Recent study reported that Bmal1-/- mice displayed many known features of premature ageing, such as reduction of bone mass. Our previous study has found that both the proliferation of bone marrow mesenchymal stem cells (BMSCs) and Bmal1 expression decreased with advancing age. It seemed that a positive correlation existed between Bmal1 protein level and the proliferative activity of BMSCs. β-catenin, the core factor of the canonical Wnt pathway, also showed reduced expression in aged mice. In order to further confirm this, we constructed a lentiviral vector to over-express Bmal1 in NIH-3T3 cells; successful transfection was verified. The cell proliferation rate of infected cells was higher than the non-transfected NIH-3T3 cells, suggesting that circadian clock gene Bmal1 can promote proliferation. β-catenin showed an increased expression in NIH-3T3 cells after Bmal1 over-expression, indicating that activation of the canonical Wnt pathway might be the mechanism underlying the effect of circadian clock gene Bmal on promoting cell proliferation.

• Combination of conventional ultrasound and elastography distinguishes breast cancers more effectively. • Combination of conventional ultrasound and elastography increases observer consistency. • BI-RADS weights more than the 2D-SWE with an increase in malignancy probability.

M2-polarized (alternatively activated) macrophages play an important role in the progression of hepatocellular carcinoma (HCC). Allograft inflammatory factor 1 (AIF1) is overexpressed in M2-polarized macrophages. This study explored the role of AIF1 in tumor-associated macrophages in HCC. Macrophages were stimulated with colony-stimulating factor 1 (CSF1) to characterize the regulatory pathway of AIF1 in macrophages. The chromatin immunoprecipitation and luciferase reporter gene assay were conducted to examine transcription factors associated with AIF1 expression. AIF1 was down or upregulated, and the effects on tumor progression were evaluated by using and co-culture systems. A cytokine array was performed to screen the downstream functional components of AIF1. Tumor tissue from 206 patients with HCC were used to explore the clinical significance of AIF1. AIF1 induced a M2-like phenotype of macrophages. By facilitating the binding of c-Jun to the promoter of AIF1, CSF1 secreted from hepatoma cells increased AIF1 expression through the CSF1R-MEK1/2-Erk1/2-c-Jun axis. AIF1 expressed in macrophages promoted the migration of hepatoma cells in co-culture system of RAW264.7 and Hepa1-6 and tumor growth in an animal model. The cytokine array showed that CXCL16 was increased in RAW264.7 cells with overexpressed AIF1, leading to enhanced tumor cell migration. In human HCC tissue, AIF1-positive macrophages in the adjacent microenvironment was associated with microvascular invasion and advanced TNM stages and with patients' overall and disease-free survival ( = 0.002 for both). AIF1 expression in macrophages plays a pivotal role in the interaction between macrophages and hepatoma cells.