molecular mechanisms by which a fucus vesiculosus extract mediates cell cycle inhibition and cell death in pancreatic cancer cells

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ID: 169616
2015
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Abstract
Pancreatic cancer is one of the most aggressive cancer entities, with an extremely poor 5-year survival rate. Therefore, novel therapeutic agents with specific modes of action are urgently needed. Marine organisms represent a promising source to identify new pharmacologically active substances. Secondary metabolites derived from marine algae are of particular interest. The present work describes cellular and molecular mechanisms induced by an HPLC-fractionated, hydrophilic extract derived from the Baltic brown seaweed Fucus vesiculosus (Fv1). Treatment with Fv1 resulted in a strong inhibition of viability in various pancreatic cancer cell lines. This extract inhibited the cell cycle of proliferating cells due to the up-regulation of cell cycle inhibitors, shown on the mRNA (microarray data) and protein level. As a result, cells were dying in a caspase-independent manner. Experiments with non-dividing cells showed that proliferation is a prerequisite for the effectiveness of Fv1. Importantly, Fv1 showed low cytotoxic activity against non-malignant resting T cells and terminally differentiated cells like erythrocytes. Interestingly, accelerated killing effects were observed in combination with inhibitors of autophagy. Our in vitro data suggest that Fv1 may represent a promising new agent that deserves further development towards clinical application.
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geisen2015marinemolecular Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Ulf Geisen;Marion Zenthoefer;Matthias Peipp;Jannik Kerber;Johannes Plenge;Antonella Managò;Markus Fuhrmann;Roland Geyer;Steffen Hennig;Dieter Adam;Levent Piker;Gerald Rimbach;Holger Kalthoff
Journal jixie gongcheng xuebao/journal of mechanical engineering
Year 2015
DOI
10.3390/md13074470
URL
http://www.mdpi.com/1660-3397/13/7/4470
Keywords
Cancer Algae autophagy fucus vesiculosus cell cycle inhibitors

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