Document Detail


The marine compound spongistatin 1 targets pancreatic tumor progression and metastasis.
MedLine Citation:
PMID:  20143389     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Treatment of pancreatic cancer remains a major challenge and new anticancer drugs are urgently required. Our study presents the marine natural compound spongistatin 1 as a promising experimental drug. Spongistatin 1 was applied in an orthotopic in vivo model of human pancreatic cancer. Spongistatin 1 significantly reduced tumor growth, which correlates with a strong apoptosis induction (DNA-fragmentation) and long-term effects on clonogenic survival of pancreatic tumor cells (L3.6pl) in vitro. In addition, the formation of metastasis was reduced in spongistatin 1-treated mice, which is in line with a diminished MMP-9 activity in tumor tissue determined by zymography. Based on the pronounced efficacy of spongistatin 1, the underlying mechanisms were studied in more detail. In vitro adhesion, as well as migration, and invasion assays showed spongistatin 1 to influence these critical steps in the metastatic cascade. Furthermore, spongistatin 1 induced anoikis in L3.6pl cells. Exposure to spongistatin 1 leads to phosphorylation, and thus inactivation of the antiapoptotic protein Bcl-2 in pancreatic tumor cells. siRNA experiments silencing Bcl-2 suggest a role of Bcl-2 in anoikis and cell migration. Taken together, spongistatin 1 not only proved to be a potent experimental drug but also served as a chemical tool to examine the role of the antiapoptotic protein Bcl-2 in pancreas carcinoma, thereby supporting the hypothesis of a link between apoptosis signaling and metastasis.
Authors:
Andrea S Rothmeier; Uta M Schneiders; Romina M Wiedmann; Ivan Ischenko; Christiane J Bruns; Anita Rudy; Stefan Zahler; Angelika M Vollmar
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  127     ISSN:  1097-0215     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-07-06     Completed Date:  2010-08-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1096-105     Citation Subset:  IM    
Affiliation:
Department of Pharmacy, Center for Drug Research, University of Munich, Munich, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoikis / drug effects
Apoptosis / drug effects
Blotting, Western
Cell Adhesion / drug effects
Cell Cycle / drug effects
Cell Movement / drug effects
Cell Proliferation / drug effects
Colony-Forming Units Assay
Female
Humans
Liver Neoplasms, Experimental / drug therapy*,  metabolism,  secondary
Lymphatic Metastasis
Macrolides / pharmacology*
Mice
Mice, Inbred BALB C
Mice, Nude
Pancreatic Neoplasms / drug therapy*,  metabolism,  pathology*
Phosphorylation / drug effects
Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors,  genetics,  metabolism*
RNA, Messenger / genetics
Reverse Transcriptase Polymerase Chain Reaction
Tubulin Modulators / pharmacology*
Xenograft Model Antitumor Assays
Chemical
Reg. No./Substance:
0/Macrolides; 0/Proto-Oncogene Proteins c-bcl-2; 0/RNA, Messenger; 0/Tubulin Modulators; 148179-94-6/spongistatin 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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