Tussilago farfara L. augments TRAIL-induced apoptosis through MKK7/JNK activation by inhibition of MKK7-TIPRL in human hepatocellular carcinoma cells = 간암세포주 Tussilago farfara L. 추출물 MKK7-TIPRL의 결합저해와 MKK7/JNK activation의 TRAIL유도 세포사멸

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dc.contributor.authorHyo Jung Lee-
dc.contributor.authorHyun Soo Cho-
dc.contributor.authorSoo Young Jun-
dc.contributor.authorJeong Ju Lee-
dc.contributor.authorJi Yong Yoon-
dc.contributor.authorJae Hye Lee-
dc.contributor.authorHyuk-Hwan Song-
dc.contributor.authorSangho Choi-
dc.contributor.authorSoo Yong Kim-
dc.contributor.authorV Saloura-
dc.contributor.authorC G Park-
dc.contributor.authorNam-Soon Kim-
dc.date.accessioned2017-04-19T09:57:51Z-
dc.date.available2017-04-19T09:57:51Z-
dc.date.issued2014-
dc.identifier.issn1021-335X-
dc.identifier.uri10.3892/or.2014.3279ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12249-
dc.description.abstractInduction of apoptosis through activation of the TRAIL pathway is considered to be a promising anticancer strategy due to its ability to selectively induce apoptosis in cancer cells. However, the ability of cancer cells to acquire TRAIL resistance has limited the clinical translation of this approach. We previously reported that the TOR signaling pathway regulator-like (TIPRL) protein contributes to the resistance to TRAIL-induced apoptosis by inhibiting the MKK7-c-Jun N-terminal kinase (JNK) pathway via MKK7?TIPRL interaction. In the present study, we identified Tussilago farfara L. (TF) as a novel TRAIL sensitizer among 500 natural products using an ELISA system that specifically detects the MKK7-TIPRL interaction, and we validated candidates by GST-pull down assay. Co-treatment of Huh7 cells with TF and TRAIL induced apoptosis via inhibition of the MKK7-TIPRL interaction and an increase in MKK7/JNK phosphorylation. This is the first report to describe TF as a novel TRAIL sensitizer, unveiling a potentially novel therapeutic strategy in cancer therapy-
dc.publisherSpandidos Publ Ltd-
dc.titleTussilago farfara L. augments TRAIL-induced apoptosis through MKK7/JNK activation by inhibition of MKK7-TIPRL in human hepatocellular carcinoma cells = 간암세포주 Tussilago farfara L. 추출물 MKK7-TIPRL의 결합저해와 MKK7/JNK activation의 TRAIL유도 세포사멸-
dc.title.alternativeTussilago farfara L. augments TRAIL-induced apoptosis through MKK7/JNK activation by inhibition of MKK7-TIPRL in human hepatocellular carcinoma cells-
dc.typeArticle-
dc.citation.titleOncology Reports-
dc.citation.number3-
dc.citation.endPage1123-
dc.citation.startPage1117-
dc.citation.volume32-
dc.contributor.affiliatedAuthorHyo Jung Lee-
dc.contributor.affiliatedAuthorHyun Soo Cho-
dc.contributor.affiliatedAuthorSoo Young Jun-
dc.contributor.affiliatedAuthorJeong Ju Lee-
dc.contributor.affiliatedAuthorJi Yong Yoon-
dc.contributor.affiliatedAuthorJae Hye Lee-
dc.contributor.affiliatedAuthorHyuk-Hwan Song-
dc.contributor.affiliatedAuthorSangho Choi-
dc.contributor.affiliatedAuthorSoo Yong Kim-
dc.contributor.affiliatedAuthorNam-Soon Kim-
dc.contributor.alternativeName이효정-
dc.contributor.alternativeName조현수-
dc.contributor.alternativeName전수영-
dc.contributor.alternativeName이정주-
dc.contributor.alternativeName윤지용-
dc.contributor.alternativeName이재혜-
dc.contributor.alternativeName송혁환-
dc.contributor.alternativeName최상호-
dc.contributor.alternativeName김수용-
dc.contributor.alternativeNameSaloura-
dc.contributor.alternativeName박춘길-
dc.contributor.alternativeName김남순-
dc.identifier.bibliographicCitationOncology Reports, vol. 32, no. 3, pp. 1117-1123-
dc.identifier.doi10.3892/or.2014.3279-
dc.subject.keywordApoptosis-
dc.subject.keywordHCC-
dc.subject.keywordMKK7-
dc.subject.keywordTIPRL-
dc.subject.keywordTRAIL resistance-
dc.subject.keywordTussilago farfara L.-
dc.subject.localapoptosis-
dc.subject.localApoptosis-
dc.subject.localHCC-
dc.subject.localMKK7-
dc.subject.localTIPRL-
dc.subject.localTRAIL resistance-
dc.subject.localTussilago farfara L.-
dc.subject.localtussilago farfara-
dc.description.journalClassY-
Appears in Collections:
Division of Research on National Challenges > Stem Cell Convergenece Research Center > 1. Journal Articles
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > International Biological Material Research Center > 1. Journal Articles
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