Abstract
Interest in marine bioresources is increasing in the drug development sector. In particular, marine sponges produce a wide range of unique metabolites that enable them to survive in challenging environments, which makes them attractive sources of candidate pharmaceuticals. In previous study, we investigated over 40 marine specimens collected in Micronesia and provided by the Korean Institute of Ocean Science and Technology, for their antiproliferative effects on various cancer cell lines, and Lipastrotethya sp. extract (LSSE) was found to have a marked antiproliferative effect. In the present study, we investigated the mechanism responsible for its anticancer effect on wild-type p53 (WT) or p53 knockout (KO) HCT116 cells. LSSE inhibited cell viability and induced apoptotic cell death more so in HCT116 p53 KO cells than the WT. HCT116 WT cells treated with LSSE underwent apoptosis associated with the induction of p53 and its target genes. On the other hand, in HCT116 p53 KO cells, LSSE reduced mTOR and Bcl-2 and increased Beclin-1 and LC3-II protein levels, suggesting autophagy induction. These results indicate that the mechanisms responsible for the anticancer effect of LSSE depend on p53 status.
Highlights
Primitive marine animals produce a diverse range of metabolites that enable them to flourish in the marine environment, and in particular, the wealth of unique metabolites produced by marine sponges has attracted the attention of those trying to develop new drugs, including anticancer drugs
We found that the marine sponge Lipastrotethya sp. (Figure 1) inhibited the proliferation of cancer cells
HCT116 and HCT116 p53KO cells were treated with Lipastrotethya sp. extract (LSSE) for 48 h and cell viability was determined using Cell Counting Kit-8
Summary
Primitive marine animals produce a diverse range of metabolites that enable them to flourish in the marine environment, and in particular, the wealth of unique metabolites produced by marine sponges has attracted the attention of those trying to develop new drugs, including anticancer drugs. Agents that induce apoptosis or autophagy are of interest as potential cancer therapies [3, 4]. Autophagy was regarded a tumor-suppressive mechanism, but it is related to tumor progression [7, 8]. These conflicting effects of autophagy depend on cancer type and the microenvironment [9]. The cell death induced by autophagy could conceivably be utilized for anticancer therapy. We investigated the mechanism responsible for its anticancer effects in HCT116 WT and HCT116 p53 KO cells
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