TGF-beta1/SMAD signaling pathway mediates p53-dependent apoptosis in hepatoma cell lines / 中国医学科学杂志(英文版)
Chinese Medical Sciences Journal
;
(4): 33-35, 2006.
Article
Dans Anglais
| WPRIM
| ID: wpr-305391
ABSTRACT
<p><b>OBJECTIVE</b>To determine whether transforming growth factor betal (TGF-beta1)/Smad signaling pathway mediates p53-dependent apoptosis in hepatoma cell lines.</p><p><b>METHODS</b>Three human hepatic carcinoma cell lines, HepG2, Huh-7, and Hep3B, were used in this study. TGF-beta1-induced apoptosis in hepatic carcinoma cell lines was analyzed using TUNEL assay. For identifying the mechanism of apoptosis induced by TGF-beta1, cell lines were transfected with a TGF-beta1-inducible luciferase reportor plasmid containing Smad4 binding elements. After transfection, cells were treated with TGF-beta1, then assayed for luciferase activity.</p><p><b>RESULTS</b>The apoptosis rate of HepG2 cell lines (48.51% +/- 8.21%) was significantly higher than control (12.72% +/- 2.18%, P <0.05). But TGF-beta1 was not able to induce apoptosis of Huh-7 and Hep3B cell lines. The relative luciferase activity of TGF-beta1-treated HepG2 cell lines (4.38) was significantly higher than control (1.00, P < 0.05). But the relative luciferase activity of TGF-beta1-treated Huh-7 and Hep3B cell lines less increased compared with control.</p><p><b>CONCLUSIONS</b>HepG2 cells seem to be highly susceptible to TGF-beta1-induced apoptosis compared with Hep3B and Huh-7 cell lines. Smad4 is a central mediator of TGF-beta1 signaling transdution pathway. TGF-beta1/Smad signaling pathway might mediate p53-dependent apoptosis in hepatoma cell lines.</p>
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Anatomopathologie
/
Pharmacologie
/
Plasmides
/
Transfection
/
Transduction du signal
/
Gènes p53
/
Apoptose
/
Gènes rapporteurs
/
Carcinome hépatocellulaire
/
Lignée cellulaire tumorale
Type d'étude:
Étude pronostique
Limites du sujet:
Humains
langue:
Anglais
Texte intégral:
Chinese Medical Sciences Journal
Année:
2006
Type:
Article
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