No abstract

Abstract. Epigallocatechin-3-gallate (EGCG) is a constituent of green tea and has been associated with anticancer activity. In the present study, the inhibitory effect of EGCG on human hepatocellular cancer cells was examined by cell viability assay, in vitro apoptosis assay and cell cycle analysis. In addition, gene expression was measured to elucidate the molecular mechanisms of action of EGCG by mitochondrial membrane potential (MMP) determination and western blot analysis. We demonstrated that EGCG induced apoptosis, decreased mitochondrial membrane potential and promoted G 0 /G 1 phase cell cycle arrest of HCCLM6 cells but not that of non-cancerous liver cells (HL-7702). The EGCG-induced apoptosis of HCCLM6 cells was associated with a significant decrease in Bcl-2 and NF-κB expression. In addition, the expression of Bax, p53, caspase-9 and caspase-3 increased, and cytochrome c was released. These results suggest that EGCG inhibits the progression of cancer through cytocidal activity and that it is a potential therapeutic compound for hepatocellular carcinoma (HCC).

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Designing a templating strategy for directing mesopore growth along different crystallographic directions is essential for fabricating two‐ or three‐dimensional single‐crystalline mesoporous zeolites. However, so far, mesopores formed in MFI zeolites by soft templates have mostly been generated by disrupting growth along the b axis; generating mesopores by disrupting growth along the a axis is rare. Herein, a single‐crystalline mesoporous MFI zeolite (SCMMZ) with sheet‐like mesopores layered along the a and b axes was synthesized using a triply branched surfactant with diquaternary ammonium groups connected to 1,3,5‐triphenylbenzene by a six‐ and eight‐carbon alkyl chain (TPB‐6 and 8). The sheet‐like mesopores were embedded in the MFI framework and were retained even after calcination. Molecular mechanics calculations provided evidence of low binding energy configurations of the surfactant that directed the growth of straight and zigzag channels along the b and a axes, respectively. The formation of nanosheets was attributed to the geometric matching of the arrangement of the aromatic groups to the zeolite framework.

No abstract

Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide and the third highest cause of cancer-related mortality in humans. Epigallocatechin-3-gallate (EGCG) has been shown to inhibit the metastatic activity of certain cancer cells. The aim of this study was to determine the effects and molecular mechanism(s) of action of EGCG in human HCC cells. A migration and invasion assay for the metastatic behavior of HCCLM6 cells was performed. The anti-metastatic effects of EGCG were investigated by RT-PCR and gelatin zymography. A total cellular protein profile was obtained using 2-dimensional gel electrophoresis (2-DE), followed by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS) analyses of proteins with significant differences in expression following treatment with EGCG. The results revealed that EGCG induced apoptosis and inhibited the metastasis of HCCLM6 cells. The anti-metastatic effects of EGCG were associated with the inhibition of matrix metalloproteinase (MMP)-2 and MMP-9 activity. The expression levels of far upstream element (FUSE) binding protein 1 (FUBP1), heat shock protein beta 1 (HSPB1), heat shock 60 kDa protein 1 (chaperonin) (CH60) and nucleophosmin (NPM) proteins, which are associated with metastasis, were significantly altered in the EGCG-treated HCCLM6 cells. The data from the present study suggest that EGCG has potential as a therapeutic agent for the treatment of HCC.

No abstract

Circular RNA carboxypeptidase A4 (circCPA4) has been shown to involve in the tumorigenesis of glioma. However, the function and the molecular mechanism of circCPA4 in glioma remain inadequate. Levels of circCPA4 and microRNA (miR)-760 were detected by quantitative real-time polymerase chain reaction. Cell proliferation, apoptosis, migration, and invasion were analyzed using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), colony formation, flow cytometry, and transwell assays, respectively. Western blot was used to detect the protein levels of matrix metallopeptidase 2 (MMP2), MMP9 and myocyte enhancer factor 2D (MEF2D). The interaction between miR-760 and circCPA4 or MEF2D was analyzed by the dual-luciferase reporter assay or RNA pull-down assay. In vivo experiments were conducted using murine xenograft models. We found circCPA4 was highly expressed in glioma, and circCPA4 knockdown suppressed tumor cell proliferative, migratory and invasive behaviors, but enhanced cell apoptosis and radiosensitivity in glioma. CircCPA4 directly bound to miR-760 to suppress its expression, and miR-760 inhibition reversed circCPA4 knockdown-mediated inhibition of cell malignant phenotypes in glioma. MEF2D was a target of miR-760, and miR-760 performed anti-tumor effects by targeting MEF2D in glioma cells. Meanwhile, we found circCPA4 could indirectly regulate MEF2D by sponging miR-760. Importantly, xenograft analysis suggested that circCPA4 knockdown impeded tumor growth in vivo via regulating miR-760 and MEF2D. In conclusion, circCPA4 knockdown suppressed cell malignant phenotypes in glioma via miR-760/MEF2D axis to impede the progression of glioma, suggesting potential therapeutic targets for glioma treatment.