scholarly journals Thyroid hormone receptor represses miR-17 expression to enhance tumor metastasis in human hepatoma cells

Oncogene ◽  
2013 ◽  
Vol 32 (38) ◽  
pp. 4509-4518 ◽  
Author(s):  
Y-H Lin ◽  
C-J Liao ◽  
Y-H Huang ◽  
M-H Wu ◽  
H-C Chi ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Tumor Metastasis ◽  
Thyroid Hormone Receptor ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells

scholarly journals Dickkopf 4 positively regulated by the thyroid hormone receptor suppresses cell invasion in human hepatoma cells

Hepatology ◽  
2012 ◽  
Vol 55 (3) ◽  
pp. 910-920 ◽  
Author(s):  
Chen-Hsin Liao ◽  
Chau-Ting Yeh ◽  
Ya-Hui Huang ◽  
Sheng-Ming Wu ◽  
Hsiang-Cheng Chi ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Cell Invasion ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells

Tri-iodothyronine and cycloheximide enhance insulin-like growth factor-binding protein-1 gene expression in human hepatoma cells

1993 ◽  
Vol 10 (1) ◽  
pp. 7-13 ◽  
Author(s):  
M Angervo ◽  
P Leinonen ◽  
R Koistinen ◽  
M Julkunen ◽  
M Seppälä
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Hepatoma Cells ◽  
Protein Synthesis Inhibitor ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Synthesis Inhibitor ◽  
Genes Encoding ◽  
Protein Mediator

ABSTRACT The growth-regulating actions of IGFs are modulated by their binding proteins (IGFBPs). The serum concentration of IGFBP-1 is down-regulated by insulin, and in-vitro studies have demonstrated that IGFBP-1 secretion from various tissues and cells can be stimulated by theophylline, forskolin, oestrogen and progesterone. We have studied the effects and mechanisms of thyroid hormone action on IGFBP-1 gene expression and secretion by human hepatoma cells in vitro. Tri-iodothyronine dose-dependently enhanced IGFBP-1 secretion in serum-free HepG2 cell cultures after 24–48 h of exposure, as measured by a specific immunofluorometric assay. This was accompanied by an increase (+ 50%) in the amount of IGFBP-1 mRNA, which could be prevented by cycloheximide, a protein synthesis inhibitor. Cycloheximide transiently enhanced (+ 200%) the accumulation of IGFBP-1 mRNA at 3–12 h of incubation, when no effect of tri-iodothyronine was observed. It is concluded that thyroid hormone stimulates IGFBP-1 secretion slowly by enhancing IGFBP-1 gene expression by a protein mediator. The acute stimulation of IGFBP-1 gene transcription by cycloheximide associates this gene with a number of growth-related genes encoding growth- and tumour-associated peptides.

scholarly journals Thyroid hormone receptors promote metastasis of human hepatoma cells via regulation of TRAIL

2012 ◽  
Vol 19 (11) ◽  
pp. 1802-1814 ◽  
Author(s):  
H-C Chi ◽  
S-L Chen ◽  
C-J Liao ◽  
C-H Liao ◽  
M-M Tsai ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptors ◽  
Hepatoma Cells ◽  
Thyroid Hormone Receptors ◽  
Human Hepatoma ◽  
Human Hepatoma Cells

scholarly journals Cathepsin H regulated by the thyroid hormone receptors associate with tumor invasion in human hepatoma cells

Oncogene ◽  
2011 ◽  
Vol 30 (17) ◽  
pp. 2057-2069 ◽  
Author(s):  
S-M Wu ◽  
Y-H Huang ◽  
C-T Yeh ◽  
M-M Tsai ◽  
C-H Liao ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Tumor Invasion ◽  
Hormone Receptors ◽  
Hepatoma Cells ◽  
Thyroid Hormone Receptors ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Cathepsin H

scholarly journals Interleukin-1β modulates endogenous thyroid hormone receptor α gene transcription in liver cells

2007 ◽  
Vol 194 (2) ◽  
pp. 257-265 ◽  
Author(s):  
J Kwakkel ◽  
W M Wiersinga ◽  
A Boelen
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Gene Transcription ◽  
Hormone Receptor ◽  
Proinflammatory Cytokine ◽  
Hepg2 Cells ◽  
Promoter Activity ◽  
Thyroid Hormone Receptor ◽  
De Novo ◽  
Hepatoma Cells

One of the main characteristics of nonthyroidal illness (NTI) is a decrease in serum triiodothyronine, partly caused by a decrease in liver deiodinase type 1 (D1) mRNA and activity. Proinflammatory cytokines have been associated with NTI in view of their capability to decrease D1 and thyroid hormone receptor (TR)β1 mRNA expression in hepatoma cells. Proinflammatory cytokine induction leads to activation of the inflammatory pathways nuclear factor (NF)κB and activator protein (AP)-1. The proinflammatory cytokine interleukin (IL)-1β decreases thyroid hormone receptor (TR)β1 mRNA in an NFκB-dependent way. The aim of this study was to unravel the effects of IL-1β on endogenous TRα gene expression in an animal model and in a liver cell line. The TRα gene product is alternatively spliced in TRα1 and TRα2, TRα2 is capable of inhibiting TRα1-induced gene transcription. We showed that both TRα1 and TRα2 mRNA decreased not only after lipopolysaccharide administration in liver of mice, but also after IL-1β stimulation of hepatoma cells (HepG2). Using the NFκB inhibitor sulfasalazine and the AP-1 inhibitor SP600125, it became clear that the IL-1β-induced decrease in TRα mRNA expression in HepG2 cells can only be abolished by simultaneous inhibition of NFκB and AP-1. The IL-1β-induced TRα1 and TRα2 mRNA decrease in HepG2 cells is the result of decreased TRα gene promoter activity, as evident from actinomycin D experiments. Cycloheximide experiments showed that the decreased promoter activity is independent of de novo protein synthesis and therefore most likely due to posttranslational modifications such as phosphorylation or subcellular relocalization.

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