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KMID : 0988920150130030233
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Intestinal Research
2015 Volume.13 No. 3 p.233 ~ p.241
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Balsalazide Potentiates Parthenolide-Mediated Inhibition of Nuclear Factor-κB Signaling in HCT116 Human Colorectal Cancer Cells
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Kim Hyun-Young
Kim Se-Lim
Park Young-Ran
Yu-Chuan Liu
Seo Seung-Young
Kim Seong-Hun
Kim In-Hee
Lee Seung-Ok
Lee Soo-Teik
Kim Sang-Wook
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Abstract
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Background/Aims: 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-κB (NF-κB) activity. Parthenolide (PT) inhibits NF-κB and exerts promising anticancer effects by promoting apoptosis. The present investigated the antitumor effects of balsalazide, combined with PT, on NF-κB in a representative human colorectal carcinoma cell line, HCT116.
Methods: 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.
Results: 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-κB p65 subunit and the phosphorylation of inhibitor of NF-κB. Moreover, PT and balsalazide dramatically enhanced NF-κB 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.
Conclusions: Combination treatment with PT and balsalazide may offer an effective strategy for the induction of apoptosis in HCT116 cells.
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KEYWORD
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Balsalazide, Parthenolide, NF-κB, Apoptosis, Colorectal neoplasms
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