Document Detail


Osteopontin regulates epithelial mesenchymal transition-associated growth of hepatocellular cancer in a mouse xenograft model.
MedLine Citation:
PMID:  22241292     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To determine the efficacy of osteopontin (OPN) targeting in hepatocellular cancer (HCC). SUMMARY/BACKGROUND: OPN is associated with HCC growth and metastasis and represents a unique therapeutic target.
METHODS: OPN and epithelial-mesenchymal transition (EMT) markers, α-smooth muscle actin (SMA), vimentin, and tenascin-c, were measured in archived human HCC tissues from metastatic (n = 4) and nonmetastatic (n = 4) settings. Additional studies utilized human Sk-Hep-1 (high OPN expression) and Hep3b (low OPN expression) HCC cells. An RNA aptamer (APT) that avidly binds (Kd = 18 nM; t1/2 = 7 hours) and ablates OPN binding was developed. Adhesion, migration/invasion, and EMT markers were determined with APT or a mutant control aptamer (Mu-APT). RFP-Luc-Sk-Hep-1 were implanted into NOD-scid mice livers and followed by using bioluminescence imaging. After verification of tumor growth, at week 3, APT (0.5 mg/kg; n = 4) or Mu-APT (0.5 mg/kg; n = 4) was injected q48h. When mice were killed at week 8, tumor cells were reisolated and assayed for EMT markers.
RESULTS: OPN and EMT markers were significantly increased in the metastatic cohort. APT inhibited Sk-Hep-1 adhesion and migration/invasion by 5- and 4-fold, respectively. APT significantly decreased EMT protein markers, SMA, vimentin, and tenascin-c. In contrast, APT did not alter Hep3B adhesion, or migration/invasion. EMT markers were slightly decreased. In the in vivo model, at weeks 6 to 8, APT inhibited HCC growth by more than 10-fold. SMA, vimentin, and tenascin-c mRNAs were decreased by 60%, 40%, and 49%, respectively, in RFP-positive Sk-Hep-1 recovered by fluorescence-activated cell sorting (P < 0.04 vs Mu-APT for all).
CONCLUSIONS: APT targeting of OPN significantly decreases EMT and tumor growth of HCC.
Authors:
Syamal D Bhattacharya; Zhiyong Mi; Victoria M Kim; Hongtao Guo; Lindsay J Talbot; Paul C Kuo
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Annals of surgery     Volume:  255     ISSN:  1528-1140     ISO Abbreviation:  Ann. Surg.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-13     Completed Date:  2012-03-20     Revised Date:  2012-05-30    
Medline Journal Info:
Nlm Unique ID:  0372354     Medline TA:  Ann Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  319-25     Citation Subset:  AIM; IM    
Affiliation:
Department of Surgery, Duke University Medical Center, Durham, NC, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Animals
Aptamers, Nucleotide
Blotting, Western
Carcinoma, Hepatocellular / metabolism*,  pathology
Cell Line, Tumor
Epithelial-Mesenchymal Transition / physiology*
Humans
Liver Neoplasms / metabolism*,  pathology
Liver Neoplasms, Experimental / metabolism,  pathology
Mice
Middle Aged
Neoplasm Metastasis
Neoplasm Transplantation
Osteopontin / metabolism*
Real-Time Polymerase Chain Reaction
SELEX Aptamer Technique
Tumor Markers, Biological / metabolism*
Grant Support
ID/Acronym/Agency:
R01 GM065113/GM/NIGMS NIH HHS; R01 GM065113/GM/NIGMS NIH HHS; R01 GM065113-05A2/GM/NIGMS NIH HHS; T32 CA093245/CA/NCI NIH HHS; T32 GM069331/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Aptamers, Nucleotide; 0/Tumor Markers, Biological; 106441-73-0/Osteopontin

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


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