The utilization of visible light for direct photocatalytic methane conversion remains a huge challenge. Here, we developed a thermo-photo catalytic process with a visible-light-responsive Pt/WO3 catalyst and realized highly efficient visible-light driven methane conversion for the first time. The conversion efficiency was enhanced by 4.6 and 14.7 times compared to room-temperature photocatalysis and thermal catalysis at 150 °C, respectively. Furthermore, the production of liquid oxygenates (mainly CH3OH) was found to proceed via photocatalysis with high apparent quantum efficiencies of 5.9%, 4.5%, and 1.9% at 350, 420, and 450 nm, respectively, while CO2 evolution was contributed by photoassisted thermal catalysis. Solid isotope evidence further confirmed that CH3OH, HCHO, and CO2 were produced via parallel rather than sequential reactions. These observations provide a valuable guide for designing a visible-light driven system for methane conversion with high efficiency and controllable selectivity.

Abstract. Metastasis of colorectal cancer (CRC) depends critically on MMP-9. KiSS-1 is a human malignant melanoma metastasis-suppressor gene. Thus, the interaction between MMP-9 and KiSS-1 has drawn considerable attention in recent years. In the present study, it was hypothesized that KiSS-1 gene could repress the metastatic potential of colorectal cancer cells by inhibiting the expression of MMP-9. Stable transfection of KiSS-1 specific siRNA and KiSS-1 expression vector in human CRC cell line HCT-116 was achieved by lentivirus infection. Moreover, the cell proliferation, invasiveness, and apoptosis were evaluated by CCK-8 method, transwell experiment, and fluorescence activated cell sorter, respectively. We also investigated the expression of MMP-9, PI3K, Akt, pAKt, and NF-кB subunit p65 using western blotting. KiSS-1 overexpression significantly decreased the cell proliferation and invasiveness of HCT-119 cells, while apoptosis was enhanced. The result of western blotting showed that synthesis of MMP-9, PI3K, p65, and phosphorylation of Akt were significantly blocked by overexpression of KiSS-1. Concatenated treatment of KiSS-1 overexpression vector with PI3K and Akt agonists attenuated the effect of KiSS-1 on the biological activity of CRC cells and also released the expression of MMP-9, PI3K, p65, and phosphorylation of Akt from the influence of overexpression of KiSS-1. Overexpression of KiSS-1 suppressed the invasiveness of CRC cells, and the gene exerted its function by reducing the expression of MMP-9 via blocking of tge PI3K/ Akt/NF-κB pathway.

Growing evidence suggests that immune-related genes (IRGs) and long non-coding RNAs (lncRNAs) can serve as prognostic markers of overall survival (OS) in patients with colon cancer. This study aimed to identify an immune-related lncRNA signature for the prospective assessment of prognosis in these patients. Gene expression and clinical data of colon cancer patients were downloaded from The Cancer Genome Atlas (TCGA). Immune-related lncRNAs were identified by a correlation analysis between IRGs and lncRNAs. In total, 447 samples were divided into a training cohort (224 samples) and a testing cohort (223 samples). Univariate, lasso and multivariate Cox regression analyses identified an immune-related nine-lncRNA signature closely related to OS in colon cancer patients in the training dataset. A risk score formula involving nine immunerelated lncRNAs was developed to evaluate the prognostic value of the lncRNA signature in the training dataset. Colon cancer patients with a high risk score had poorer OS than those with a low risk score. A multivariate Cox regression analysis confirmed that the immune-related nine-lncRNA signature could be an independent prognostic factor in colon cancer patients. The results were further confirmed in the testing cohort and the entire TCGA cohort. Furthermore, a gene set enrichment analysis revealed several pathways with significant enrichment in the high-and low-risk groups that may be helpful in formulating clinical strategies and understanding the underlying mechanisms. Finally, a quantitative real-time polymerase chain reaction assay found that the nine lncRNAs were significantly differentially expressed in colon cancer cell lines. The results of this study indicate that this signature has important clinical implications for improving predictive outcomes and guiding individualized treatment in colon cancer patients. These lncRNAs could be potential biomarkers affecting the prognosis of colon cancer.

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Photocatalytic ethane conversion into value-added chemicals is a great challenge especially under visible light irradiation. The production of ethyl hydroperoxide (CH3CH2OOH), which is a promising radical reservoir for regulating the...

These data suggest that KISS1 is down-regulated in cancer tissues via promoter hypermethylation and therefore may represent a candidate target for treating metastatic CRC.

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Cardiac fibrosis is a deleterious effect of many cardiovascular diseases. Previous studies have shown that curcumin has exhibited protective effects on cardiovascular diseases. The aim of the present study was to evaluate the effects of curcumin on the activity of human cardiac fibroblasts (CFs) and to elucidate the underlying mechanisms involved. Human CFs were incubated with or without curcumin (20 µmol/l) and transforming growth factor β1 (TGF-β1; 10 ng/ml), and the expression of α-smooth muscle actin (α-SMA), collagen type Iα (COLA)-1 and COLA3 was evaluated using reverse transcription-quantitative polymerase chain reaction and western blot analysis. Cell proliferation was evaluated by Cell Counting Kit-8 analysis, and phases of the cell cycle were studied by flow cytometry. Western blot analysis was performed to evaluate the expression of cyclin-dependent kinase 1 (CDK1), Cyclin B, phosphorylation (p)-mothers against decapentaplegic homolog 2/3 (p-smad2/3), p-P38, and p-extracellular regulated protein kinases (ERK). Curcumin significantly reduced mRNA and protein levels of α-SMA, COLA1, and COLA3 in CFs stimulated with TGF-β1. However, in the absence of TGF-β1, curcumin did not have any effects on CFs, suggesting that curcumin inhibited TGF-β1-mediated CF activities, including differentiation and collagen deposition. Additionally, curcumin inhibited the proliferation of TGF-β1-treated CFs, and promoted G2/M phase cell cycle arrest. Curcumin reduced cell cycle protein expression by inhibiting smad2/3, p38 mitogen-activated protein kinase, and ERK phosphorylation in TGF-β1-treated CFs. Thus, these results indicated that curcumin may be a potential anti-fibrotic drug to treat cardiac fibrosis.