Document Detail


Cellular metabolic responses of PET radiotracers to (188)Re radiation in an MCF7 cell line containing dominant-negative mutant p53.
MedLine Citation:
PMID:  17499732     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We investigated the relations between the cell uptakes of metabolic radiotracers and beta-radiation pretreatment using a dominant mutant p53 (p53mt) cell line to evaluate the effects of p53 genes on (18)F labeled positron emission tomography (PET) radiotracer uptakes. METHODS: pCMV-Neo-Bam (control), which contains a neo-resistance marker, and p53 dominant-negative mutant expression constructs were stably transfected into MCF7 cell line. Cells were plated in 24-well plates at 1.0x10(5) cells for 18 h. Rhenium-188 ((188)Re) (a beta emitter) was added to the medium (3.7, 18.5, 37 MBq) and incubated for 24 h. We performed gamma-counting to determine the cellular uptakes of 2-[(18)F]fluoro-2-deoxy-d-glucose (FDG), o-(2-[(18)F]fluoroethyl)-l-tyrosine (FET) and 2'-[(18)F]fluoro-2'-deoxythymidine (FLT) (370 kBq, 60 min). Cell viabilities were determined by trypan blue staining and flow cytometry. RESULTS: p53mt cells showed 1.5-2-fold higher FDG uptake than wild-type p53 cells in basal condition, and the difference of FDG uptake was greater after (188)Re treatment (P<.01). FET uptake increased with (188)Re dose without a significant difference between p53 statuses. p53mt cells showed lower FLT uptake than wild-type p53 cells in basal condition, and the difference of FLT uptake was greater after (188)Re treatment. By cell viability testing and FACS analysis, p53mt cells showed lower viability and a larger apoptotic fraction (sub-G1) than wild-type p53 cells after (188)Re treatment. CONCLUSION: We speculate that p53 dysfunction increases glucose and decreases thymidine metabolism in cancer cells and that this may be exaggerated by (188)Re beta-radiation. Our findings suggest that FDG could reflect tumor viability and malignant potential after (188)Re beta-radiation treatment, whereas FLT could be a more useful PET radiotracer for assessing therapeutic response to beta-radiation, especially in cancer cells with an altered function of p53.
Authors:
Gi Jeong Cheon; Hye-Kyung Chung; Jung-A Choi; Su-Jae Lee; Soon-Hyuk Ahn; Tae-Sup Lee; Chang Woon Choi; Sang Moo Lim
Publication Detail:
Type:  Journal Article     Date:  2007-03-30
Journal Detail:
Title:  Nuclear medicine and biology     Volume:  34     ISSN:  0969-8051     ISO Abbreviation:  Nucl. Med. Biol.     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-05-14     Completed Date:  2007-08-13     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9304420     Medline TA:  Nucl Med Biol     Country:  England    
Other Details:
Languages:  eng     Pagination:  425-32     Citation Subset:  IM    
Affiliation:
Laboratory of Nuclear Medicine Research, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, South Korea. larry@kcch.re.kr
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MeSH Terms
Descriptor/Qualifier:
Amino Acids / biosynthesis
Apoptosis / drug effects,  radiation effects
Beta Particles
Blotting, Western
Cell Line, Tumor
Cell Survival / drug effects,  radiation effects
Cells / metabolism*,  radiation effects*
DNA / biosynthesis
Flow Cytometry
Fluorodeoxyglucose F18 / pharmacokinetics,  pharmacology
Genes, p53 / genetics*
Glucose / biosynthesis
Hexokinase / metabolism
Humans
Positron-Emission Tomography
Radioisotopes
Radiopharmaceuticals / pharmacokinetics*
Rhenium*
Transfection
Chemical
Reg. No./Substance:
0/Amino Acids; 0/Radioisotopes; 0/Radiopharmaceuticals; 50-99-7/Glucose; 63503-12-8/Fluorodeoxyglucose F18; 7440-15-5/Rhenium; 9007-49-2/DNA; EC 2.7.1.1/Hexokinase

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


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