Article
Expression of IAPs and alternative splice variants in hepatocellular carcinoma tissues and cells.
Dipartimento di Scienze Farmacologiche, Università di Palermo, Via del Vespro 129, 90127 Palermo, Italy.
Annals of the New York Academy of Sciences (impact factor:
3.15).
01/2005;
1028:289-93.
DOI:10.1196/annals.1322.033
pp.289-93
Source: PubMed
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Citations (0)
- Cited In (1)
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Article: [Down-regulation of survivin in growth inhibition of hepatoma cells induced by a selective cyclooxygenase-2 inhibitor].
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ABSTRACT: Cyclooxygenase-2 (COX-2) inhibitors reportedly inhibit the growth of hepatocellular carcinoma (HCC) via caspase-dependent or caspase-independent apoptosis, which is due to COX-2 being associated with hepatocarcinogenesis. Survivin is highly expressed in most human cancers, but the mechanism regulating survivin expression remains unclear. We investigated the regulatory expression of survivin in selective-COX-2-inhibitor-induced growth inhibition of hepatoma cells. After treatment with NS-398 (a selective COX-2 inhibitor) at various concentrations (10, 50, 100, 150, and 200 micrometer), the growth inhibition of Hep3B hepatoma cells was assessed by an MTT cell-viability assay, DNA fragmentation gel analysis, and flow cytometry. The expression of survivin transcript was analyzed by reverse-transcription polymerase chain reactions. NS-398 inhibited the growth of hepatoma cells by an amount dependent on the concentration and the time since treatment. Apoptotic DNA ladder and flow-cytometry shifting to the sub-G1 phase were revealed in NS-398-induced growth inhibition of hepatoma cells. NS-398 suppressed the expression of the survivin gene in a concentration- and time-dependent manner. Survivin was down-regulated in the growth inhibition of hepatoma cells induced by a selective COX-2 inhibitor, NS-398, in a concentration- and time-dependent manner. These results suggest the therapeutic inhibition of COX-2 via suppression of survivin in HCC.The Korean Journal of Hepatology 10/2008; 14(3):351-9.
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Keywords
alternative splice variants
apoptosis proteins
coordinated expression
different IAPs
human HCC
IAPs
major role
marks
present results
tumor
unfavorable prognosis
XIAP