Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1998-3-4
|
| pubmed:abstractText |
Tumor cells expressing the herpes simplex virus-thymidine kinase (HSV-tk) gene become sensitive to ganciclovir (GCV), and the phenomenon by which tumor cells surrounding the HSV-tk expressing cells also become sensitive to GCV is known as the "bystander effect." The purpose of this study was to investigate the bystander effect in human lung-cancer cell lines, and the role of gap-junctional intercellular communication as the mechanism responsible for it. Gap-junctional intercellular communication was measured both with a dye-transfer assay involving single-cell microinjection of Lucifer Yellow and with a PKH26/calcein-AM double-dye-transfer assay. Significant bystander tumoricidal effect was observed in lung-cancer cell lines when cultured cells contained only 10% HSV-tk expressing cells. This was also observed to occur with cell lines of different origin or from different species. Although gap-junctional intercellular communication characterized by rapid transfer of Lucifer Yellow was not observed, we did detect gap-junctional communication marked by the slow transfer of calcein-AM in lung-cancer cell lines. However, neither an inhibitor (1-octanol) nor an enhancer (all trans-retinoic acid [ATRA]) of gap-junctional communication affected the extent of the bystander effect. These findings suggest that low levels of gap-junctional communication may be efficient for producing the bystander effect in lung-cancer cells, or that other mechanisms may underlie this effect. Although gap-junctional communication may play an important role in generating the bystander effect in tumor cells expressing the HSV-tk gene, further knowledge of the mechanism of this effect may help improve the treatment of lung cancer with an HSV-tk system.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-Octanol,
http://linkedlifedata.com/resource/pubmed/chemical/Antimetabolites, Antineoplastic,
http://linkedlifedata.com/resource/pubmed/chemical/Ganciclovir,
http://linkedlifedata.com/resource/pubmed/chemical/Thymidine Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
1044-1549
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
18
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
205-12
|
| pubmed:dateRevised |
2006-4-21
|
| pubmed:meshHeading |
pubmed-meshheading:9476907-1-Octanol,
pubmed-meshheading:9476907-Animals,
pubmed-meshheading:9476907-Antimetabolites, Antineoplastic,
pubmed-meshheading:9476907-Carcinoma,
pubmed-meshheading:9476907-Cell Communication,
pubmed-meshheading:9476907-Cell Division,
pubmed-meshheading:9476907-Cell Transformation, Viral,
pubmed-meshheading:9476907-Coculture Techniques,
pubmed-meshheading:9476907-Ganciclovir,
pubmed-meshheading:9476907-Gap Junctions,
pubmed-meshheading:9476907-Genetic Vectors,
pubmed-meshheading:9476907-Humans,
pubmed-meshheading:9476907-Lung Neoplasms,
pubmed-meshheading:9476907-Mice,
pubmed-meshheading:9476907-Moloney murine leukemia virus,
pubmed-meshheading:9476907-Simplexvirus,
pubmed-meshheading:9476907-Thymidine Kinase,
pubmed-meshheading:9476907-Tretinoin,
pubmed-meshheading:9476907-Tumor Cells, Cultured
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Bystander tumoricidal effect and gap junctional communication in lung cancer cell lines.
|
| pubmed:affiliation |
First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
|
| pubmed:publicationType |
Journal Article
|