Studies on the Mechanism of Hypoxic Increase of VEGF Expression in the Hep3B Human Hepatoma Cells / 대한암학회지
Journal of the Korean Cancer Association
;
: 220-226, 1997.
Article
Dans Coréen
| WPRIM
| ID: wpr-123102
ABSTRACT
PURPOSE:
Hepatocellular carcinoma (HCC), a typical hypervasculized tumor is very sensitive to hypoxia and vascular endothelial growth factor (VEGF) has previously been identified to be up-regulated in response to hypoxia in several cell types. However, the molecular mechanisms by which hypoxia is sensed by the cells remain enigmatic. To investigate whether calcium and AP-1 are involved in hypoxia-sensing mechanism, we performed following experiments. MATERIALS ANDMETHODS:
Hep3B cells were grown in hypoxic condition. To assess cell viability, MTT assay was performed. To investigate the effect of calcium and AP-1, northern blot analysis was performed after treatment with BAPTA/AM.RESULTS:
The expression of VEGF was significantly up-regulated by hypoxia in Hep3B, hepatocellular carcinoma cell line. The increased expression of VEGF induced by hypoxia was blocked by the addition of BAPTA/AM, a cytosolic calcium chelator to the media. In addition, we found that the expression of c-jun protooncogene was also up-regulated by hypoxia. Hypoxic increase of c-jun expression was also normalized by the treatment with BAPTA/AM.CONCLUSION:
These results suggest that the increased expression of VEGF by hypoxia is mediated through the calcium and c-jun signalling pathway in the Hep3B human hepatoma cell lines.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Lignée cellulaire
/
Survie cellulaire
/
Technique de Northern
/
Calcium
/
Carcinome hépatocellulaire
/
Facteur de transcription AP-1
/
Cytosol
/
Facteur de croissance endothéliale vasculaire de type A
/
Hypoxie
Type d'étude:
Étude pronostique
Limites du sujet:
Humains
langue:
Coréen
Texte intégral:
Journal of the Korean Cancer Association
Année:
1997
Type:
Article
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