Agarum clathratum (A. clathratum) is a marine brown algal species that belongs to the Costariaceae family and has antioxidant and anti-microbial properties. However, the anti-inflammatory effects of A. clathratum and the molecular mechanisms involved have not been determined so far. This study aimed to investigate the anti-inflammatory effects of A. clathratum extracts in THP-1 macrophages stimulated by lipopolysaccharide (LPS) derived from Porphyromonas gingivalis. The THP-1 cells were differentiated with 12-O-tetradecanoylphorbol-13-acetate and treated with A. clathratum before LPS stimulation. Cell viability was assessed using the trypan blue exclusion assay. The expression of pro-inflammatory response-associated molecules was evaluated by quantitative real-time polymerase chain reaction and Western blot analysis. A. clathratum treatment inhibited the expression of interleukin-1β in LPS-stimulated THP-1 macrophages without causing any cytotoxicity. The anti-inflammatory effect of A. clathratum resulted in a significant repression of the JNK/c-Jun signaling axis, a key regulator in inflammation responses. This study highlights the possible role of A. clathratum in the inhibition of pro-inflammatory cytokines via suppression of the JNK/c-Jun signaling axis and suggests that A. clathratum could serve as a marine-derived anti-inflammatory agent in periodontitis.

Background: Cisplatin is a well-known platinum-containing anti-cancer drug against bladder, ovarian, lung and testicular cancer. However, the potential effects and molecular targets of cisplatin in human mucoepidermoid carcinoma (MEC) are not fully understood. Here, we investigated the apoptotic effect and underlying mechanism of cisplatin in human MEC cells. Methods: The potential effects of cisplatin were evaluated by trypan blue exclusion assay, Western blotting, 4’-6-diamidino-2-phenylindole (DAPI) staining, live/dead assay and immunocytochemistry. Results: Cisplatin suppressed cell growth and enhanced expression of cleaved PAPR in MC3 and YD15 cells. Cisplatin caused morphological change of nuclei and increased the number of ethidium homodimer-1-stained cells. In addition, cisplatin commonly increased Bax activation in both cells, while other Bcl-2 family proteins were not affected. Conclusions: These results suggest that cisplatin might induce apoptosis by activating Bax protein, which would provide baseline data for development of effective treatment strategy against MEC.

Background. Vitamin K (VK) is a fat-soluble vitamin and is known to have anticancer activity in various cancer cell lines. However, there is no report on the anticancer effect of VK2 in mucoepidermoid carcinoma cells. Methods. The effects of VK2 on anti-proliferative and apoptotic activity were recognized by the trypan blue exclusion assay, 4'-6-diamidino-2-phenylindole (DAPI) staining and Western blot analysis. Results. The results showed that VK2 decreased cell viability and induced apoptotic programmed cell death in MC3 cells evidenced by the cleavages of caspase3 and PARP. VK2 treatment clearly increased Bak and truncated Bid (t-Bid) compared with the control treatment whereas it did not alter other Bcl-2 family members. Conclusions. Overall, our results suggest that VK2 can be a good apoptotic inducer accompanied by the increase in Bak and Bid protein. VK2 may be a potent target of anticancer drug candidate for the treatment of oral cancer.

The human embryonic-lethal abnormal vision-like protein, HuR, stabilizes mRNA containing adenine- and uridine- rich elements in their 3’untranslated region. Because cyclooxygenase-2 (COX-2) mRNA is a cellular transcript that contains an adenine- and uridine-rich element, it can be regulated by the HuR protein. In this study, we examined the relationship between COX-2, HuR, MVD, and the clinicopathological parameters. Nineteen out of 43 cases of HNSCC showed high level of COX-2expression, and 68% of these patients showed high COX-2 immuno-reactivity indicating the strong expression of the cytoplasmic HuR protein. Also, MVD expression in the cases with high COX-2 expression was higher than in the cases with low COX-2 expression. These results suggest a strong correlation between the overexpression of cytoplasmic HuR and COX-2 expression in HNSCC, and that COX-2 is associated with MVD in HNSCC. In conclusion, COX-2 regulated by cytoplasmic HuR may be a good tumor angiogenic factor in HNSCC.