Abstract | AIM: METHODS: TXNIP expression was measured by quantitative reverse transcription polymerase chain reaction and western blots. TXNIP expression was stimulated by vitamin D exposure and by transfection. Cell proliferation, apoptosis and reactive oxygen species were determined by standard assays. RESULTS: TXNIP expression levels were low in HCC cell lines, and vitamin D3 stimulated TXNIP expression in vitro. In HCC cells transfected with a TXNIP expression vector or treated with exogenous vitamin D3, there was a reduction in cell proliferation and an increase in apoptosis. Cells expressing TXNIP were markedly susceptible to oxidative injury induced by cobalt chloride or bacterial lipopolysaccharide. TXNIP expression was reduced or absent in a majority of primary human HCC specimens relative to matching, non-cancerous liver tissue. CONCLUSION: TXNIP expression is low or absent in human HCC specimens and HCC-derived cell lines. Vitamin D3 stimulates TXNIP expression, resulting in diminished proliferation and enhanced apoptosis. Liver cells expressing TXNIP are primed for oxidative injury. These findings suggest that stimulation of TXNIP expression, by factors such as vitamin D3, may attenuate carcinogenesis in patients with chronic liver disease.
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Authors | James P Hamilton, James J Potter, Lahari Koganti, Stephen J Meltzer, Esteban Mezey |
Journal | Hepatology research : the official journal of the Japan Society of Hepatology
(Hepatol Res)
Vol. 44
Issue 13
Pg. 1357-66
(Dec 2014)
ISSN: 1386-6346 [Print] Netherlands |
PMID | 24451003
(Publication Type: Journal Article)
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Copyright | Published 2014. This article is a U.S. Government work and is in the public domain in the USA. |