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• W2079111811 startingPage "6698" @default.
• W2079111811 abstract "Bortezomib, a proteasome inhibitor, has been clinically approved for the treatment of myeloma and lymphoma. Here, we report a differential effect of bortezomib on apoptosis in four hepatocellular carcinoma (HCC) cell lines and identify the major molecular event that determines sensitivity. Although bortezomib inhibited proteasome activity to a similar extent in all HCC cell lines, it showed differential effects on their viability: Huh-7 (IC(50) 196 nmol/L), Sk-Hep1 (IC(50) 180 nmol/L), Hep3B (IC(50) 112 nmol/L), and resistant PLC5 (IC(50) >1,000 nmol/L). Bortezomib caused cell cycle arrest at G(2)-M phase in all HCC cells tested whereas apoptotic induction was found only in sensitive cells but not in PLC5 cells. No significant bortezomib-induced NF-kappaB changes were noted in Huh-7 and PLC5. Bortezomib down-regulated phospho-Akt (P-Akt) in a dose- and time-dependent manner in all sensitive HCC cells whereas no alterations of P-Akt were found in PLC5. Down-regulation of Akt1 by small interference RNA overcame the apoptotic resistance to bortezomib in PLC5 cells, but a constitutively activated Akt1 protected Huh-7 cells from bortezomib-induced apoptosis. Furthermore, bortezomib showed suppression of tumor growth with down-regulation of P-Akt in Huh-7 tumors but not in PLC5 tumors. Down-regulation of P-Akt represents a major molecular event of bortezomib-induced apoptosis in HCC cell lines and may be a biomarker for predicting clinical response to HCC treatment. Targeting Akt signaling overcomes drug resistance to bortezomib in HCC cells, which provides a new approach for the combinational therapy of HCC." @default.
• W2079111811 created "2016-06-24" @default.
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• W2079111811 date "2008-08-12" @default.
• W2079111811 modified "2023-10-18" @default.
• W2079111811 title "Down-regulation of Phospho-Akt Is a Major Molecular Determinant of Bortezomib-Induced Apoptosis in Hepatocellular Carcinoma Cells" @default.
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• W2079111811 doi "https://doi.org/10.1158/0008-5472.can-08-0257" @default.
• W2079111811 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18701494" @default.
• W2079111811 hasPublicationYear "2008" @default.
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