Curcumin (diferuloylmethane), widely used as a spice and coloring agent in food, possesses potent antioxidant, anti-inflammatory and anticarcinogenic properties. Recently, curcumin was further demonstrated to have an antimetastatic effect in mice. In this study, we attempted to clarify the possible mechanisms of this latter effect of curcumin. A highly invasive SK-Hep-1 cell line of human hepatocellular carcinoma (HCC) was selected for this study. An in vitro assay, without or with Matrigel matrix, was used to quantitate cellular migration and invasion. Gelatin-based zymography was adapted to assay the secretion of matrix metalloproteinase (MMP). We found that curcumin, at 10 µM, inhibited 17.4 and 70.6% of cellular migration and invasion of SK-Hep-1, respectively. Compared with a less invasive human HCC cell line, Huh-7, SK-Hep-1 showed a much higher MMP-9 secretion. Further, and parallel with its anti-invasion activity, curcumin inhibited MMP-9 secretion in SK-Hep-1 in a dose-dependent fashion. We conclude that curcumin has a significant anti-invasion activity in SK-Hep-1 cells, and that this effect is associated with its inhibitory action on MMP-9 secretion.

To discover the new medical entity from edible marine algae, our continuously natural product investigation focused on endophytes from marine macroalgae Grateloupia sp. Two new azaphilones, 8a-epi-hypocrellone A (1), 8a-epi-eupenicilazaphilone C (2), together with five known azaphilones, hypocrellone A (3), eupenicilazaphilone C (4), ((1E,3E)-3,5-dimethylhepta-1,3-dien-1-yl)-2,4-dihydroxy-3-methylbenzaldehyde (5), sclerotiorin (6), and isochromophilone IV (7) were isolated from the alga-derived fungus Penicillium sclerotiorum. The structures of isolated azaphilones (1–7) were elucidated by spectrometric identification, especially HRESIMS, CD, and NMR data analyses. Concerning bioactivity, cytotoxic, anti-inflammatory, and anti-fibrosis activities of those isolates were evaluated. As a result, compound 1 showed selective toxicity toward neuroblastoma cell line SH-SY5Y among seven cancer and one fibroblast cell lines. 20 μM of compounds 1, 3, and 7 inhibited the TNF-α-induced NFκB phosphorylation but did not change the NFκB activity. Compounds 2 and 6 respectively promoted and inhibited SMAD-mediated transcriptional activities stimulated by TGF-β.

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