Intest Res.  2015 Jul;13(3):233-241. 10.5217/ir.2015.13.3.233.

Balsalazide Potentiates Parthenolide-Mediated Inhibition of Nuclear Factor-kappaB Signaling in HCT116 Human Colorectal Cancer Cells

  • 1Department of Internal Medicine, Medical School of Chonbuk National University, Jeonju, Korea.
  • 2Colon Carcinogenesis and Inflammation Laboratory, Biomedical Research Institute of Chonbuk National University Hospital, Jeonju, Korea.


Balsalazide is an anti-inflammatory drug used in the treatment of inflammatory bowel disease. Balsalazide can reduce inflammatory responses via several mechanisms, including inhibition of nuclear factor-kappaB (NF-kappaB) activity. Parthenolide (PT) inhibits NF-kappaB and exerts promising anticancer effects by promoting apoptosis. The present investigated the antitumor effects of balsalazide, combined with PT, on NF-kappaB in a representative human colorectal carcinoma cell line, HCT116.
We counted cells and conducted annexin-V assays and cell cycle analysis to measure apoptotic cell death. Western blotting was used investigate the levels of proteins involved in apoptosis.
PT and balsalazide produced synergistic anti-proliferative effects and induced apoptotic cell death. The combination of balsalazide and PT markedly suppressed nuclear translocation of the NF-kappaB p65 subunit and the phosphorylation of inhibitor of NF-kappaB. Moreover, PT and balsalazide dramatically enhanced NF-kappaB p65 phosphorylation. Apoptosis, through the mitochondrial pathway, was confirmed by detecting effects on Bcl-2 family members, cytochrome c release, and activation of caspase-3 and -8.
Combination treatment with PT and balsalazide may offer an effective strategy for the induction of apoptosis in HCT116 cells.


Balsalazide; Parthenolide; NF-kappaB; Apoptosis; Colorectal neoplasms
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