A novel derivative of decursin, CSL-32, blocks migration and production of inflammatory mediators and modulates PI3K and NF-kappa B activities in HT1080 cells
- Authors
- Lee, Seung-Hee; Lee, Jee Hyun; Kim, Eun-Ju; Kim, Won-Jung; Suk, Kyoungho; Kim, Joo-Hwan; Song, Gyu Yong; Lee, Won-Ha
- Issue Date
- Jul-2012
- Publisher
- WILEY-BLACKWELL
- Keywords
- cytokine; inflammation; invasion; NF-kappa B; signal transduction
- Citation
- CELL BIOLOGY INTERNATIONAL, v.36, no.7, pp.683 - 688
- Journal Title
- CELL BIOLOGY INTERNATIONAL
- Volume
- 36
- Number
- 7
- Start Page
- 683
- End Page
- 688
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16301
- DOI
- 10.1042/CBI20110257
- ISSN
- 1065-6995
- Abstract
- Decursin and related coumarin compounds in herbal extracts have a number of biological activities against inflammation, angiogenesis and cancer. We have analysed a derivative of decursin (CSL-32) for activity against inflammatory activation of cancer cells, such as migration, invasion and expression of pro-inflammatory mediators. The human fibrosarcoma cell line, HT1080, was treated with TNF alpha (tumour necrosis factor alpha) in the presence or absence of CSL-32. The cellular responses and modification of signalling adapters were analysed with respect to the production of pro-inflammatory mediators, as also migration, adhesion and invasion. Treatment of HT1080 cells with CSL-32 inhibited their proliferation, without affecting cell viability, and TNF alpha-induced expression of pro-inflammatory mediators, such as MMP-9 (matrix metalloproteinase-9) and IL-8 (interleukin-8). CSL-32 also suppressed phosphorylation and degradation of I kappa B (inhibitory kappa B), phosphorylation of p65 subunit of NF-kappa B (nuclear factor-kappa B) and nuclear translocation of NF-kappa B, which are required for the expression of pro-inflammatory mediators. In addition, CSL-32 inhibited invasion and migration of HT1080 cells, as also cellular adhesion to fibronectin, an ECM (extracellular matrix) protein. CSL-32 treatment resulted in a dose-dependent inhibition of PI3K (phosphoinositide 3-kinase) activity, required for the cellular migration. The analyses show that CSL-32 inhibits processes associated with inflammation, such as the production of pro-inflammatory mediators, as well as adhesion, migration and invasion in HT1080 cells.
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