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Title   간암세포에서 저산소증에 의해 유도되는 VEGF의 발현기작에 대한 연구 ( Studies on the Mechanism of Hypocix Increase of VEGF Expression in the Hep3B Human Hepatoma Cells )
Publicationinfo   1997 Jan; 029(02): 220-227.
Key_word   Hypoxia, Hep3B cell, VEGF, Calcium, c-jun
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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 and Methods: 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.
저 자   권유욱(Yu Wook Kwon),배수경(Soo Kyung Bae),김정애(Jung Ae Kim),김규원(Kyu Won Kim),박병채(Byung Chae Park)