Document Detail


Effect of prostaglandin E2-producing nonmetastatic Lewis lung carcinoma cells on the migration of prostaglandin E2-responsive metastatic Lewis lung carcinoma cells.
MedLine Citation:
PMID:  3109729     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The role of prostaglandin E2 (PGE2) in directly stimulating metastatic spread by Lewis lung carcinoma (LLC) cells was examined with the use of an in vitro migration model for tumor dissemination. The extent to which cloned metastatic and nonmetastatic LLC cells migrated out of glass capillary tubes in vitro reflected their capacity to form pulmonary metastases in vivo. The addition of PGE2 to metastatic LLC cells further stimulated their migration. Other cyclooxygenase products, besides PGE2, did not stimulate the migration of metastatic LLC cells. Nonmetastatic LLC cells did not migrate out of capillary tubes, even in the presence of exogenous PGE2. The amount of PGE2 secreted by cloned LLC cells was quantitated by a radioimmunoassay. Nonmetastatic LLC cells secreted more PGE2 than did the metastatic LLC cells. When the nonmetastatic LLC cells were either mixed with or placed adjacent to cloned metastatic LLC cells, the migration by the metastatic LLC cells was stimulated. The migration-stimulatory capacity of the nonmetastatic LLC cells was minimized in the presence of indomethacin, a prostaglandin synthesis inhibitor. Studies were conducted to relate these in vitro results to tumor metastasis in vivo. Injection of a mixture of metastatic and nonmetastatic LLC cells into mice s.c. resulted in a greater number of lung metastases than did injection of metastatic cells alone. This increase in metastasis formation was prevented by indomethacin. Formation of pulmonary metastases was also augmented when irradiated nonmetastatic LLC cells were injected into metastatic LLC-bearing mice. The results of our studies suggest that nonmetastatic LLC cells, by producing PGE2, can augment in vitro migration and in vivo dissemination of metastatic LLC cells. Thus, the response of tumor cells to PGE2, rather than simply their production of PGE2, appears to be important in regulating tumor dissemination.
Authors:
M R Young; M E Young; H T Wepsic
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  47     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  1987 Jul 
Date Detail:
Created Date:  1987-08-20     Completed Date:  1987-08-20     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  3679-83     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
16,16-Dimethylprostaglandin E2 / pharmacology
Animals
Clone Cells
Dinoprostone
Indomethacin / pharmacology
Lung Neoplasms / metabolism*
Mice
Mice, Inbred C57BL
Neoplasm Metastasis*
Prostaglandin-Endoperoxide Synthases / metabolism
Prostaglandins E / biosynthesis*
Radioimmunoassay
Grant Support
ID/Acronym/Agency:
CA39371/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Prostaglandins E; 363-24-6/Dinoprostone; 39746-25-3/16,16-Dimethylprostaglandin E2; 53-86-1/Indomethacin; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases

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


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