29 329

Cited 0 times in

Sulfasalazine induces apoptosis of HBx-expressing cells in an NF-kappaB-independent manner.

Authors
Lee, YM; Kang, M; Hwang, JM; Lee, S; Cho, H; Kim, YS
Citation
Virus genes, 40(1):37-43, 2010
Journal Title
Virus genes
ISSN
0920-85691572-994X
Abstract
The Hepatitis B virus (HBV) is a causative agent of acute chronic hepatitis, cirrhosis, and hepatocarcinoma. The Hepatitis B virus X protein (HBx) has pleiotypic functions in the regulation of proliferation and apoptosis. It has been suggested that the anti-inflammatory drug sulfasalazine, which is commonly used to treat rheumatoid arthritis and inflammatory bowel disease, inhibits nuclear factor NF-kappaB and induces cell death in HBx-expressing liver cells. In this study, we demonstrate that sulfasalazine induces cell death via apoptosis in HBx-expressing liver cells, as evidenced by characteristic changes in nuclear morphology, cleavage of poly (ADP-ribose) polymerase (PARP), caspase-3 and caspase-9, and activation of caspase-3. We also demonstrate that inhibition of NF-kappaB by siRNA fails to induce apoptosis of HBx-expressing liver cells, indicating that sulfasalazine modulates apoptosis of HBx-expressing cells in an NF-kappaB-independent manner.
MeSH terms
Apoptosis/drug effects*Caspase 3/metabolismCaspase 9/metabolismCell LineEnzyme Activation/drug effectsHepatitis B virus/metabolism*HumansLiver/cytologyLiver/drug effectsLiver/metabolismNF-kappa B/geneticsNF-kappa B/metabolism*Poly(ADP-ribose) Polymerases/metabolismSulfasalazine/pharmacology*Trans-Activators/geneticsTrans-Activators/metabolism*
DOI
10.1007/s11262-009-0416-4
PMID
19859796
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
조, 혜성
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse