간암세포에서 저산소증에 의해 유도되는 VEGF의 발현기작에 대한 연구
Studies on the Mechanism of Hypoxic Increase of VEGF Expression in the Hep3B Human Hepatoma Cells
대한암학회지 1997년 29권 2호 p.220 ~ 226
소속 상세정보
권유욱
배수경/김정애/김규원/박병채
KMID : 0360319970290020220
Abstract
Purpose:
@EN 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.
@ES Materials and Methods:
@EN 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 BATPA/AM.
@ES Results:
@EN 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 BATPA/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.
@ES Conclusion:
@EN 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.
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