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1.
Chinese Journal of Hepatology ; (12): 191-195, 2011.
Article Dans Chinois | WPRIM | ID: wpr-290605

Résumé

<p><b>OBJECTIVE</b>To investigate the role of miR-221/222 in inhibiting endoplasmic reticulum stress-induced human hepatocarcinoma cells apoptosis.</p><p><b>METHOD</b>miR-221/222 mimics and inhibitors were used to mimic or block the function of endogenous miR-221/222 respectively. Western blot and flow cytometry were used to test the effects of miR-221/222 on cell cycle and apoptosis under endoplasmic reticulum stress in human hepatocellular carcinoma cells.</p><p><b>RESULTS</b>Endoplasmic reticulum stress resulted in miR-221/222 down-regulation in human hepatocellular carcinoma cells. miR-221/222 mimics and inhibitors inhibited and promoted respectively endoplasmic reticulum stress-mediated p27Kip1 induction. Moreover, p27Kip1 suppression not only resulted in reduction in the fraction of G1 phase cells, but also promoted the endoplasmic reticulum stress-mediated apoptosis in human hepatocellular carcinoma cells.</p><p><b>CONCLUSION</b>miR-221/222 were downregulated by endoplasmic reticulum stress in human hepatocellular carcinoma cells, which subsequently protected human hepatocellular carcinoma cells against endoplasmic reticulum stress-induced apoptosis through p27Kip1 regulation.</p>


Sujets)
Humains , Apoptose , Carcinome hépatocellulaire , Métabolisme , Anatomopathologie , Cycle cellulaire , Lignée cellulaire tumorale , Inhibiteur p27 de kinase cycline-dépendante , Métabolisme , Réticulum endoplasmique , Métabolisme , Tumeurs du foie , Métabolisme , Anatomopathologie , microARN , Métabolisme
2.
Chinese Journal of Hepatology ; (12): 909-914, 2010.
Article Dans Chinois | WPRIM | ID: wpr-360799

Résumé

<p><b>OBJECTIVE</b>To investigate the cross-talk between the PI3K/Akt and MEK/ERK pathways and its role in cell cycle regulation under endoplasmic reticulum stress in human hepatocellular carcinoma cells.</p><p><b>METHODS</b>PI3K inhibitor LY294002 and MEK inhibitor U0126 were used to block the PI3K/Akt and MEK/ERK pathways respectively, and constitutively activated Akt mutant construct was used to activate the PI3K/Akt pathway. Western blot was used to study the potential cross-talk between the PI3K/Akt and MEK/ERK pathways under endoplasmic reticulum stress in human hepatocellular carcinoma cells. the role of the cross-talk between the PI3K/Akt and MEK/ERK pathways in cell cycle regulation was investigated by using propidium iodide staining.</p><p><b>RESULTS</b>LY294002 not only blocked Akt activation efficiently but also increased ERK phosphorylation markedly under endoplasmic reticulum stress in SMMC-7721 and Hep3B cells. Furthermore, myr-Akt inhibited endoplasmic reticulum stress-mediated ERK phosphorylation. In contrast, MEK inhibitor U0126 had no effect on endoplasmic reticulum stress-induced Akt activation. It is notable that both myr-Akt overexpression and MEK inhibitor U0126 inhibited endoplasmic reticulum stress-induced G0/G1 phase arrest in SMMC-7721 cells.</p><p><b>CONCLUSION</b>Endoplasmic reticulum stress-induced Akt activation is mediated through PI3K and the PI3K/Akt pathway inactivation is involved in increased ERK activity in human hepatocellular carcinoma cells. The cross-talk between the PI3K/Akt and MEK/ERK cascades plays an important role in endoplasmic reticulum stress-induced human hepatocellular carcinoma cell cycle arrest.</p>


Sujets)
Humains , Butadiènes , Pharmacologie , Carcinome hépatocellulaire , Métabolisme , Cycle cellulaire , Lignée cellulaire tumorale , 4H-1-Benzopyran-4-ones , Pharmacologie , Réticulum endoplasmique , Métabolisme , Extracellular Signal-Regulated MAP Kinases , Métabolisme , Mitogen-Activated Protein Kinase Kinases , Métabolisme , Morpholines , Pharmacologie , Nitriles , Pharmacologie , Phosphatidylinositol 3-kinase , Métabolisme , Phosphorylation , Protéines proto-oncogènes c-akt , Métabolisme , Transduction du signal
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