Hepatocyte growth factor enhances protein phosphatase Cdc25A inhibitor compound 5-induced hepatoma cell growth inhibition via Akt-mediated MAPK pathway

2005 ◽  
Vol 203 (3) ◽  
pp. 510-519 ◽  
Author(s):  
Ziqiu Wang ◽  
Meifang Wang ◽  
Brian I. Carr
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Hepatocyte Growth Factor ◽  
Growth Inhibition ◽  
Protein Phosphatase ◽  
Mapk Pathway ◽  
Hepatoma Cell ◽  
Cell Growth Inhibition ◽  
Hepatocyte Growth

scholarly journals Association of v-ErbA with Smad4 Disrupts TGF-β Signaling

2009 ◽  
Vol 20 (5) ◽  
pp. 1509-1519 ◽  
Author(s):  
Richard A. Erickson ◽  
Xuedong Liu
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Transforming Growth Factor ◽  
Mechanistic Explanation ◽  
Transforming Growth Factor Β ◽  
Cell Growth Inhibition ◽  
Erythroleukemia Cells ◽  
Avian Erythroblastosis Virus

Disruption of the transforming growth factor-β (TGF-β) pathway is observed in the majority of cancers. To further understand TGF-β pathway inactivation in cancer, we stably expressed the v-ErbA oncoprotein in TGF-β responsive cells. v-ErbA participates in erythroleukemic transformation of cells induced by the avian erythroblastosis virus (AEV). Here we demonstrate that expression of v-ErbA was sufficient to antagonize TGF-β–induced cell growth inhibition and that dysregulation of TGF-β signaling required that v-ErbA associate with the Smad4 which sequesters Smad4 in the cytoplasm. We also show that AEV-transformed erythroleukemia cells were resistant to TGF-β–induced growth inhibition and that TGF-β sensitivity could be recovered by reducing v-ErbA expression. Our results reveal a novel mechanism for oncogenic disruption of TGF-β signaling and provide a mechanistic explanation of v-ErbA activity in AEV-induced erythroleukemia.

scholarly journals Mediation of the inhibitory effect of thyroid hormone on proliferation of hepatoma cells by transforming growth factor-beta

2006 ◽  
Vol 36 (1) ◽  
pp. 9-21 ◽  
Author(s):  
Chun-Che Yen ◽  
Ya-Hui Huang ◽  
Chu-Yu Liao ◽  
Cheng-Jung Liao ◽  
Wan-Li Cheng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Thyroid Hormone ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Transforming Growth Factor ◽  
Cyclin E ◽  
Hepatoma Cell ◽  
Stable Cell Line ◽  
Mrna Levels

Thyroid hormone (triiodothyronine, T3) regulates growth, development and differentiation. To examine the influence of T3 on hepatoma cell growth, thyroid receptor (TR)α1 or TRβ1 over-expressing HepG2 cell lines were used. Growth of the HepG2-TR stable cell line was inhibited by over 50% following treatment with T3. However, transforming growth factor (TGF)-β neutralizing antibody, but not the control antibody can reverse the cell growth inhibition effect of T3. Flow cytometric analysis indicated that the growth inhibition was apparent at the transition point between the G1 and S phases of the cell cycle. The expression of major cell cycle regulators was used to provide further evidence for the growth inhibition. Cyclin-dependent kinase 2 (cdk2) and cyclin E were down-regulated in HepG2-TR cells. Moreover, p21 protein or mRNA levels were up-regulated by around 5-fold or 7.3-fold respectively following T3 treatment. Furthermore, phospho-retinoblastoma (ppRb) protein was down-regulated by T3. The expression of TGF-β was studied to delineate the repression mechanism. TGF-β was stimulated by T3 and its promoter activity was enhanced six- to eight-fold by T3. Furthermore, both T3 and TGF-β repressed the expression of cdk2, cyclin E and ppRb. On the other hand, TGF-β neutralizing but not control antibody blocked the repression of cdk2, cyclin E and ppRb by T3. These results demonstrated that T3 might play a key role in liver tumor cell proliferation.

The antifibrogenic effect of hepatocyte growth factor (HGF) on renal tubular (HK-2) cells is dependent on cell growth

2009 ◽  
Vol 27 (3) ◽  
pp. 173-180 ◽  
Author(s):  
Ciro Esposito ◽  
Bina Parrilla ◽  
Flavia Cornacchia ◽  
Fabrizio Grosjean ◽  
Filippo Mangione ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Hepatocyte Growth Factor ◽  
Antifibrogenic Effect ◽  
Renal Tubular ◽  
Hepatocyte Growth
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