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

• Published in: Virus genes Vol. 40; no. 1; pp. 37 - 43
• Main Authors: Lee, Young-Man, Kang, Moonkyung, Hwang, Jung-Me, Lee, Sukyung, Cho, Hyeseong, Kim, Yeon-Soo
• Format: Journal Article
• Language: English
• Published: New York Boston : Springer US 01.02.2010; Springer US
• Subjects: apoptosis; Biomedical and Life Sciences; Biomedicine; caspase-3; caspase-9; chronic hepatitis; Hepatitis B virus; hepatocytes; inflammatory bowel disease; Medical Microbiology; Plant Sciences; rheumatoid arthritis; small interfering RNA; Virology; NF-κB; Sulfasalazine; HBx; Apoptosis
• ISSN: 0920-8569; 1572-994X
• DOI: 10.1007/s11262-009-0416-4

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-κB 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-κB by siRNA fails to induce apoptosis of HBx-expressing liver cells, indicating that sulfasalazine modulates apoptosis of HBx-expressing cells in an NF-κB-independent manner.