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DC Field | Value | Language |
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dc.citation.endPage | 1750 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 1740 | - |
dc.citation.title | CANCER RESEARCH | - |
dc.citation.volume | 66 | - |
dc.contributor.author | Kim, H | - |
dc.contributor.author | Kim, EH | - |
dc.contributor.author | Eom, YW | - |
dc.contributor.author | Kim, WH | - |
dc.contributor.author | Kwon, TK | - |
dc.contributor.author | Lee, SJ | - |
dc.contributor.author | Choi, KS | - |
dc.date.accessioned | 2023-12-22T10:08:07Z | - |
dc.date.available | 2023-12-22T10:08:07Z | - |
dc.date.created | 2016-08-02 | - |
dc.date.issued | 2006-02 | - |
dc.description.abstract | Sulforaphane is a chemopreventive agent present in various cruciferous vegetables, including broccoli. Here, we show that treatment with tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in combination with subtoxic doses of sulforaphane significantly induces rapid apoptosis in TRAIL-resistant hepatoma cells. Neither TNF-alpha- nor Fas-mediated apoptosis was sensitized in hepatoma cells by cotreatment with sulforaphane, suggesting that sulforaphane can selectively sensitize cells to TRAIL-induced apoptosis but not to apoptosis mediated by other death receptors. We found that sulforaphane treatment significantly up-regulated mRNA and protein levels of DR5, a death receptor of TRAIL. This was accompanied by an increase in the generation of reactive oxygen species (ROS). Pretreatment with N-acetyl-L-cysteine and overexpression of catalase inhibited sulforaphane-induced up-regulation of DR5 and almost completely blocked the cotreatment-induced apoptosis. Furthermore, the sulforaphane-mediated sensitization to TRAIL was efficiently reduced by administration of a blocking antibody or small interfering RNAs for DR5. These results collectively indicate that sulforaphane-induced generation of ROS and the subsequent up-regulation of DR5 are critical for triggering and amplifying TRAIL-induced apoptotic signaling. We also found that sulforaphane can sensitize both Bcl-xL- and Bcl-2-overexpressing hepatoma cells to TRAIL-induced apoptosis, indicating that treatment with a combination of TRAIL and sulforaphane may be a safe strategy for treating resistant hepatomas | - |
dc.identifier.bibliographicCitation | CANCER RESEARCH, v.66, no.3, pp.1740 - 1750 | - |
dc.identifier.doi | 10.1158/0008-5472.CAN-05-1568 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.scopusid | 2-s2.0-32944475745 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/20184 | - |
dc.identifier.url | http://cancerres.aacrjournals.org/content/66/3/1740 | - |
dc.identifier.wosid | 000235095900061 | - |
dc.language | 영어 | - |
dc.publisher | AMER ASSOC CANCER RESEARCH | - |
dc.title | Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-resistant hepatoma cells to TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of DR5 | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | HUMAN HEPATOCELLULAR-CARCINOMA | - |
dc.subject.keywordPlus | DEATH RECEPTOR 5/TRAIL-R2 | - |
dc.subject.keywordPlus | COLON-CANCER CELLS | - |
dc.subject.keywordPlus | CYCLE ARREST | - |
dc.subject.keywordPlus | BCL-XL | - |
dc.subject.keywordPlus | ANTITUMOR-ACTIVITY | - |
dc.subject.keywordPlus | DECOY RECEPTORS | - |
dc.subject.keywordPlus | DOWN-REGULATION | - |
dc.subject.keywordPlus | P53 GENE | - |
dc.subject.keywordPlus | IN-VITRO | - |
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