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Can some marine-derived fungal metabolites become actual anticancer agents?
Gomes, N.; Lefranc, F.; Kijjoa, A.; Kiss, R. (2015). Can some marine-derived fungal metabolites become actual anticancer agents? Mar. Drugs 13(6): 3950-3991. http://dx.doi.org/10.3390/md13063950
In: Marine Drugs. Molecular Diversity Preservation International (MDPI): Basel. ISSN 1660-3397, more
Peer reviewed article  

Available in  Authors 

Keywords
Author keywords
    marine fungi; natural products; anticancer; chemotherapeutic; cytotoxic;multidrug resistance; in vivo antitumor; non-apoptotic; pro-apoptotic;preclinical

Authors  Top 
  • Gomes, N.
  • Lefranc, F.
  • Kijjoa, A.
  • Kiss, R., more

Abstract
    Marine fungi are known to produce structurally unique secondary metabolites, and more than 1000 marine fungal-derived metabolites have already been reported. Despite the absence of marine fungal-derived metabolites in the current clinical pipeline, dozens of them have been classified as potential chemotherapy candidates because of their anticancer activity. Over the last decade, several comprehensive reviews have covered the potential anticancer activity of marine fungal-derived metabolites. However, these reviews consider the term “cytotoxicity” to be synonymous with “anticancer agent”, which is not actually true. Indeed, a cytotoxic compound is by definition a poisonous compound. To become a potential anticancer agent, a cytotoxic compound must at least display (i) selectivity between normal and cancer cells (ii) activity against multidrug-resistant (MDR) cancer cells; and (iii) a preferentially non-apoptotic cell death mechanism, as it is now well known that a high proportion of cancer cells that resist chemotherapy are in fact apoptosis-resistant cancer cells against which pro-apoptotic drugs have more than limited efficacy. The present review thus focuses on the cytotoxic marine fungal-derived metabolites whose ability to kill cancer cells has been reported in the literature. Particular attention is paid to the compounds that kill cancer cells through non-apoptotic cell death mechanisms.

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