Activation of AMP-activated protein kinase (AMPK), a physiological cellular energy sensor, strongly suppresses cell proliferation in both nonmalignant and tumor cells. This study demonstrates the mechanism of quercetin-induced apoptosis in HT-29 colon cancer cells. Treatment of cells with quercetin significantly decreased cell viability in a dose-dependent manner. Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group. All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.

Landfill gas (LFG), which is primarily composed of CH(4), CO(2), and N(2), is produced from the anaerobic digestion of organic materials. To investigate the feasibility of the storage and transportation of LFG via the formation of hydrate, we observed the phase equilibrium behavior of CO(2)-CH(4)-N(2) mixture hydrates. When the specific molar ratio of CO(2)/CH(4) was 40/55, the equilibrium dissociation pressures were gradually shifted to higher pressures and lower temperatures as the mole fraction of N(2) increased. X-ray diffraction revealed that the CO(2)-CH(4)-N(2) mixture hydrate prepared from the CO(2)/CH(4)/N(2) (40/55/5) gas mixture formed a structure I clathrate hydrate. A combination of Raman and solid-state (13)C NMR measurements provided detailed information regarding the cage occupancy of gas molecules trapped in the hydrate frameworks. The gas storage capacity of LFG hydrates was estimated from the experimental results for the hydrate formations under two-phase equilibrium conditions. We also confirmed that trace amounts of nonmethane organic compounds do not affect the cage occupancy of gas molecules or the thermodynamic stability of LFG hydrates.

The CO2-, CH4-, and CO2/CH4-loaded β-form hydroquinone (HQ) clathrates were synthesized by the gas-phase reaction between α-form HQ and high pressure gases. Temperature-dependent Raman spectra of guest-free, CO2-loaded, CH4-loaded, and CO2/CH4-loaded β-form HQ clathrates were measured in the temperature range 300–385 K at increments of 5 K. The CH4 molecules rapidly escaped from the β-form HQ clathrate in the temperature range 360–380 K, whereas the CO2 molecules were gradually released from the β-form HQ clathrate framework in the wide temperature range 300–380 K. It was also found that both CO2 and CH4 molecules were rapidly released from the CO2/CH4-loaded β-form HQ clathrate framework in the temperature range 360–380 K. However, all of the guest-free and guest-loaded β-form HQ clathrates were fully converted to the α-form HQ at the same temperature of 385 K. These results demonstrate the strong effect of temperature on both guest–host interactions and the stability of the framework structure.

Sulforaphane [1-isothiocyanato-4-(methylsulfinyl)-butane] is an isothiocyanate found in some cruciferous vegetables, especially broccoli. Sulforaphane has been shown to display anti-cancer properties against various cancer cell lines. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in cancer cell invasion. In this study, we investigated the effect of sulforaphane on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced MMP-9 expression and cell invasion in MCF-7 cells. TPA-induced MMP-9 expression and cell invasion were decreased by sulforaphane treatment. TPA substantially increased NF-κB and AP-1 DNA binding activity. Pre-treatment with sulforaphane inhibited TPA-stimulated NF-κB binding activity, but not AP-1 binding activity. In addition, we found that sulforaphane suppressed NF-κB activation, by inhibiting phosphorylation of IκB in TPA-treated MCF-7 cells. In this study, we demonstrated that the inhibition of TPA-induced MMP-9 expression and cell invasion by sulforaphane was mediated by the suppression of the NF-κB pathway in MCF-7 cells. [BMB Reports 2013; 46(4): 201-206]

The data demonstrate that cyanidin-3-glucoside isolated from mulberry induced apoptosis in breast cancer (MDA-MB-453) cells, and therefore, has a potential as an anti-cancer agent. These results show that mulberry cyanidin-3-glucoside inhibit the proliferation and growth in vitro and in vivo model and, indicating the inhibition of tumor progression.