Novel Anti-Melanoma Compounds Are Efficacious in A375 Cell Line Xenograft Melanoma Model in Nude Mice.

Despite the successes of immunotherapy, melanoma remains one of the deadliest cancers, therefore, the need for innovation remains high. We previously reported anti-melanoma compounds that work by downregulating spliceosomal proteins hnRNPH1 and H2. In a separate study, we reported that these compounds were non-toxic to Balb/C mice at 50 mg/kg suggesting their utility in in vivo studies.

In Vivo Acute Toxicity Studies of Novel Anti-Melanoma Compounds Downregulators of hnRNPH1/H2.

Despite the recent advances in melanoma therapy, the need for new targets and novel approaches to therapy is urgent. We previously reported melanoma actives that work via binding and downregulating spliceosomal proteins hnRNPH1 and H2. Given the lack of knowledge about the side effects of using spliceosomal binders in humans, an acute toxicity study was conducted to evaluate these compounds in mice.

Radioprotective efficacy of dieckol against gamma radiation-induced cellular damage in hepatocyte cells.

Naturally occurring antioxidants prevent or delay the harmful effect of free radical formation and radioprotection. The present study aimed to investigate the radioprotective effect of dieckol, a naturally occurring marine bioactive phenolic compound on lipid peroxidation and antioxidant status, DNA damage, and inflammation in gamma-radiation-induced rat primary hepatocytes. Isolated hepatocyte cells exposed to gamma-radiation showed an increased level of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) accompanied with the decrease in the activities of enzymatic (SOD, CAT, and GPx) and non-enzymatic (vitamin C, vitamin E, and GSH) antioxidants associated with increased DNA damage coupled with upregulation of inflammatory proteins (NF-κB and COX-2) compared to control.

Modulatory efficacy of dieckol on xenobiotic-metabolizing enzymes, cell proliferation, apoptosis, invasion and angiogenesis during NDEA-induced rat hepatocarcinogenesis.

Dieckol (DEK) is a major polyphenol of marine brown seaweed Ecklonia cava which is a potential candidate for cancer therapy. However, the underlying mechanism of DEK as an anticancer drug remains to be elucidated. In this study, we evaluated the molecular mechanisms involved in the chemopreventive efficacy of DEK in N-nitrosodiethylamine (NDEA)-induced hepatocarcinogenesis rats by analyzing markers of xenobiotic-metabolizing enzymes (XMEs), apoptosis, invasion, and angiogenesis.

Protective effects of dieckol on N-nitrosodiethylamine induced hepatocarcinogenesis in rats.

Dieckol (DEK) is a naturally occuring phlorotannins found in marine brown algae Ecklonia cava which is attributed with various pharmacological properties. This study was aimed to investigate the protective role of DEK on N-Nitrosdiethylamine (NDEA) induced rat hepatocarcinogenesis. In this investigation 0.