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Biotech / Medical : TITAN PHARMACEUTICAL (TTP)
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To: scaram(o)uche who wrote (68)6/20/1999 5:07:00 PM
From: scaram(o)uche  Read Replies (1) of 362
 
more parking.......

Br J Cancer 1999 May;80(5-6):705-10

Sodium butyrate enhances STAT 1 expression in PLC/PRF/5 hepatoma
cells and augments their responsiveness to interferon-alpha.

Hung WC, Chuang LY

School of Technology for Medical Sciences, Kaohsiung Medical College, Taiwan, Republic of China.

[Medline record in process]

Although interferon-alpha (IFN-alpha) has shown great promise in the treatment of chronic viral hepatitis, the anti-tumour effect
of this agent in the therapy of liver cancer is unclear. Recent studies have demonstrated that differentiation-inducing agents could
modulate the responsiveness of cancer cells to IFN-alpha by regulating the expression of signal transducers and activators of
transcription (STAT) proteins, a group of transcription factors which play important roles in the IFN signalling pathway. We
have reported that sodium butyrate is a potent differentiation inducer for human hepatoma cells. In this study, we investigated
whether this drug could regulate the expression of STAT proteins and enhance the anti-tumour effect of IFN-alpha in hepatoma
cells. We found that sodium butyrate specifically activated STAT1 gene expression and enhanced IFN-alpha-induced
phosphorylation and activation of STAT1 proteins. Co-treatment with these two drugs led to G1 growth arrest, accompanied
by down-regulation of cyclin D1 and up-regulation of p21WAF-1, and accumulation of hypophosphorylated retinoblastoma
protein in hepatoma cells. Additionally, internucleosomal DNA fragmentation, a biological hallmark of apoptosis, was detected
in hepatoma cells after continuous incubation with a combination of these two drugs for 72 h. Our results show that sodium
butyrate potently enhances the anti-tumour effect of IFN-alpha in vitro and suggest that a rational combination of these two
drugs may be useful for the treatment of liver cancer.
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