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
DC Field | Value | Language |
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dc.contributor.author | Lee, Seung-Hee | - |
dc.contributor.author | Lee, Jee Hyun | - |
dc.contributor.author | Kim, Eun-Ju | - |
dc.contributor.author | Kim, Won-Jung | - |
dc.contributor.author | Suk, Kyoungho | - |
dc.contributor.author | Kim, Joo-Hwan | - |
dc.contributor.author | Song, Gyu Yong | - |
dc.contributor.author | Lee, Won-Ha | - |
dc.date.available | 2020-02-29T05:46:31Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2012-07 | - |
dc.identifier.issn | 1065-6995 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16301 | - |
dc.description.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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | WILEY-BLACKWELL | - |
dc.relation.isPartOf | CELL BIOLOGY INTERNATIONAL | - |
dc.subject | VEGF-INDUCED ANGIOGENESIS | - |
dc.subject | ANGELICA-GIGAS | - |
dc.subject | CARCINOMA-CELLS | - |
dc.subject | PROSTATE-CANCER | - |
dc.subject | IN-VIVO | - |
dc.subject | ACTIVATION | - |
dc.subject | ANGELATE | - |
dc.subject | BETA | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | MACROPHAGES | - |
dc.title | 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 | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000306161300013 | - |
dc.identifier.doi | 10.1042/CBI20110257 | - |
dc.identifier.bibliographicCitation | CELL BIOLOGY INTERNATIONAL, v.36, no.7, pp.683 - 688 | - |
dc.identifier.scopusid | 2-s2.0-84862856897 | - |
dc.citation.endPage | 688 | - |
dc.citation.startPage | 683 | - |
dc.citation.title | CELL BIOLOGY INTERNATIONAL | - |
dc.citation.volume | 36 | - |
dc.citation.number | 7 | - |
dc.contributor.affiliatedAuthor | Kim, Joo-Hwan | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | cytokine | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | invasion | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | signal transduction | - |
dc.subject.keywordPlus | VEGF-INDUCED ANGIOGENESIS | - |
dc.subject.keywordPlus | ANGELICA-GIGAS | - |
dc.subject.keywordPlus | CARCINOMA-CELLS | - |
dc.subject.keywordPlus | PROSTATE-CANCER | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | ANGELATE | - |
dc.subject.keywordPlus | BETA | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | MACROPHAGES | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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