scholarly journals The role of hypoxia response element in TGFβ-induced carbonic anhydrase IX expression in Hep3B human hepatoma cells

2017 ◽  
Vol 69 (4) ◽  
pp. 593-601
Author(s):  
Hatice Yildirim ◽  
Merve Karaman ◽  
Feray Köçkar
2001 ◽  
Vol 188 (2) ◽  
pp. 188-193 ◽  
Author(s):  
Hui-Chiu Chang ◽  
Li-Huang Tsai ◽  
Lea-Yea Chuang ◽  
Wen-Chun Hung

2011 ◽  
Author(s):  
Chin-Wen Chi ◽  
Ming-Ta Sung ◽  
Ann-Tin Ho ◽  
Chin-Chun Lee ◽  
Wei-Shan Tu ◽  
...  

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 14081-14081
Author(s):  
M. Li ◽  
S. Zhou ◽  
X. Liu ◽  
G. Li

14081 Background: This study was to explored the functional mechanism of alpha-fetoprotein (AFP) in maintaining the proliferation of human hepatoma cells line Bel 7402 and the immunsuppression of lymphocyte Jurkat cells. Methods: Western blot was used to detecting the expression of some apoptosis-related gene, fluorescence labeled AFP and confocal microscopy scanning for receptor binding assay in the membrane in Jurkat cells. Results: It showed that AFP could enhance the expression of survivin and c-ras, but restrain caspase-3 express in Bel 7402 cells by Western blotting analysis. It also showed that AFP could bind to the membrane of Jurkat cells by confocal microscopy scanning, and when treated Jurkat with AFP, it indicated that AFP could repress the expression of survivin and Livin and elevated the activity of caspase-3 in the cells; Co-cultured Bel 7402 cells with Jurkat cells, the expression of tumor necrosis related-apoptosis induced ligand (TRAIL) in Jurkt cells was inhibited, when pretreatment with monoclonal antibody of AFP (Anti-AFP), the restrained effect of TRAIL express and the activity of caspase-3 was elevated in Jurkat cells was removed. It also indicated that Anti-AFP had an ability to block these functions of AFP. Conclusions: AFP has a capability to promote the growth and escape from immune surveillance of human hepatoma cells through enhancing the expression of ras and survivin gene in Bel 7402 cells, suppressing TRAIL, survivin and Livin expressed and upregulated activity of caspase-3 in Jurkat cells. No significant financial relationships to disclose.


2010 ◽  
Vol 249 (3) ◽  
pp. 224-230 ◽  
Author(s):  
Guo-Dong Zhou ◽  
Molly Richardson ◽  
Inayat S. Fazili ◽  
Jianbo Wang ◽  
Kirby C. Donnelly ◽  
...  

1993 ◽  
Vol 290 (3) ◽  
pp. 819-825 ◽  
Author(s):  
K Mitani ◽  
H Fujita ◽  
Y Fukuda ◽  
A Kappas ◽  
S Sassa

The role of inorganic metals and metalloporphyrins in the induction of mRNAs for haem oxygenase and heat-shock protein 70 (hsp70), the two heat-shock proteins, was examined in human HepG2 and Hep3B hepatoma cells. SnCl2, but not Sn-protoporphyrin, was found to be a potent inducer of both haem oxygenase and hsp70 mRNAs. In contrast, CoCl2, ZnCl2 and FeCl2 caused little induction of haem oxygenase and hsp70 mRNAs, whereas the porphyrin complexes of these metals strongly induced haem oxygenase mRNA, without influencing the level of hsp70 mRNA. The induction process was largely transcriptional, as judged by the inhibition of induction by actinomycin D, but not by cycloheximide, and by increased transcription demonstrated by nuclear run-off analysis. Since CoCl2 is a potent inducer of haem oxygenase in vivo in animals, the possibility of the biosynthesis of Co-protoporphyrin was examined in human hepatoma cells by incubating them with CoCl2 and protoporphyrin, or delta-aminolaevulinate (ALA), the precursor of protoporphyrin. Both types of treatment led to a potent induction of haem oxygenase mRNA. Co-protoporphyrin formation was also spectrally demonstrated in cells incubated with the metal and ALA. The results of this study indicate that certain metals, e.g. SnCl2, may directly induce haem oxygenase mRNA, whereas with other elements, incorporation of the metal into the porphyrin macrocycle is necessary for induction. Therefore CoCl2, like haemin, may activate the haem oxygenase gene via a haem-responsive transcription factor, whereas SnCl2 may exert its effect via a metal-responsive transcription factor.


1991 ◽  
Vol 11 (6) ◽  
pp. 3001-3008
Author(s):  
K A Won ◽  
H Baumann

The 142-bp cytokine response element of the rat alpha 1-acid glycoprotein (AGP) gene is a complex of several additively contributing regulatory sequences. By using deletions and point mutations, a minimal interleukin-1 (IL-1) response element was localized to the region from positions 1 to 36 within the 5'-most AB fragment of the cytokine response element. Two distinct sequence motifs were contained within this element, both of which were required to achieve full IL-1 response in rat and human hepatoma cells. This element showed a minor response to phorbol ester treatment only in human hepatoma cells. Southwestern (DNA-protein) blot analysis of nuclear proteins of rat liver and hepatoma cells revealed the presence of a heat-labile nuclear factor (NF-AB). NF-AB migrated as a basic protein with an apparent molecular mass of 37 kDa and bound specifically to the DNA sequence at positions 10 to 37 of the AB fragment. The NF-AB binding activity was detected neither in the cytoplasmic fraction of rat hepatoma cells nor in nuclear extracts from control or acute-phase rat kidney. The binding activity of NF-AB correlated with the transcriptional activity of the endogenous AGP gene in rat liver and hepatoma cells. Nuclear extract from human HepG2 cells showed a similar binding activity with an apparent molecular mass of 34.5 kDa. The human NF-AB binding activity was detectable only after 13 h of cytokine treatment and was not induced by phorbol ester. Tissue distribution, DNA sequence binding specificity, and kinetics of cytokine induction of NF-AB do not coincide with the characteristics of any other described factors that have been associated with cytokine regulation. Therefore, NF-AB is considered a new candidate involved in IL-1 regulation of the rat AGP gene.


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