Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/94029
DC FieldValueLanguage
dc.contributor.authorLiu, Shing-Hwazh_TW
dc.contributor.authorLee, Wen-Janezh_TW
dc.contributor.authorLai, De-Weizh_TW
dc.contributor.authorWu, Sheng-Maozh_TW
dc.contributor.authorLiu, Chia-Yuzh_TW
dc.contributor.authorTien, Hsing-Ruzh_TW
dc.contributor.authorChiu, Chien-Shanzh_TW
dc.contributor.authorPeng, Yen-Chunzh_TW
dc.contributor.authorJan, Yee-Jeezh_TW
dc.contributor.authorChao, Te-Hsinzh_TW
dc.contributor.authorPan, Hung-Chuanzh_TW
dc.contributor.authorSheu, Meei-Lingzh_TW
dc.date2015-04-
dc.date.accessioned2016-08-08T07:14:43Z-
dc.date.available2016-08-08T07:14:43Z-
dc.identifier.urihttp://hdl.handle.net/11455/94029-
dc.description.abstractPeritoneal dissemination is a major clinical obstacle in gastrointestinal cancer therapy, and it accounts for the majority of cancer-related mortality. Calreticulin (CRT) is over-expressed in gastric tumors and has been linked to poor prognosis. In this study, immunohistochemistry studies revealed that the up-regulation of CRT was associated with lymph node and distant metastasis in patients with gastric cancer specimens. CRT was significantly down-regulated in highly metastatic gastric cancer cell lines and metastatic animal by Honokiol-treated. Small RNA interference blocking CRT by siRNA-CRT was translocated to the cells in the early immunogenic response to Honokiol. Honokiol activated endoplasmic reticulum (ER) stress and down-regulated peroxisome proliferator-activated receptor-γ (PPARγ) activity resulting in PPARγ and CRT degradation through calpain-II activity, which could be reversed by siRNA-calpain-II. The Calpain-II/PPARγ/CRT axis and interaction evoked by Honokiol could be blocked by gene silencing or pharmacological agents. Both transforming growth factor (TGF)-β1 and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induced cell migration, invasion and reciprocal down-regulation of epithelial marker E-cadherin, which could be abrogated by siRNA-CRT. Moreover, Honokiol significantly suppressed MNNG-induced gastrointestinal tumor growth and over-expression of CRT in mice. Knockdown CRT in gastric cancer cells was found to effectively reduce growth ability and metastasis in vivo. The present study provides insight into the specific biological behavior of CRT in epithelial-to-mesenchymal transition (EMT) and metastasis. Taken together, our results suggest that the therapeutic inhibition of CRT by Honokiol suppresses both gastric tumor growth and peritoneal dissemination by dictating early translocation of CRT in immunogenic cell death, activating ER stress, and blocking EMT.zh_TW
dc.language.isoenzh_TW
dc.relationMolecular oncology, Volume 9, Issue 4, Page(s) 834-49.zh_TW
dc.subjectCalreticulinzh_TW
dc.subjectCarcinogenesiszh_TW
dc.subjectEndoplasmic reticulum stresszh_TW
dc.subjectEpithelial-to-mesenchymal transitionzh_TW
dc.subjectImmunogenic cell deathzh_TW
dc.subjectAdultzh_TW
dc.subjectAnimalszh_TW
dc.subjectBiomarkers, Tumorzh_TW
dc.subjectBiphenyl Compoundszh_TW
dc.subjectCalpainzh_TW
dc.subjectCalreticulinzh_TW
dc.subjectCell Deathzh_TW
dc.subjectCell Line, Tumorzh_TW
dc.subjectDown-Regulationzh_TW
dc.subjectEndoplasmic Reticulum Stresszh_TW
dc.subjectEpithelial-Mesenchymal Transitionzh_TW
dc.subjectFemalezh_TW
dc.subjectGene Knockdown Techniqueszh_TW
dc.subjectHumanszh_TW
dc.subjectLignanszh_TW
dc.subjectMacrophageszh_TW
dc.subjectMalezh_TW
dc.subjectMethylnitronitrosoguanidinezh_TW
dc.subjectMice, Inbred BALB Czh_TW
dc.subjectMice, Inbred C57BLzh_TW
dc.subjectMiddle Agedzh_TW
dc.subjectNeoplasm Invasivenesszh_TW
dc.subjectPPAR gammazh_TW
dc.subjectPhagocytosiszh_TW
dc.subjectPromoter Regions, Geneticzh_TW
dc.subjectProtein Bindingzh_TW
dc.subjectStomach Neoplasmszh_TW
dc.subjectUp-Regulationzh_TW
dc.titleHonokiol confers immunogenicity by dictating calreticulin exposure, activating ER stress and inhibiting epithelial-to-mesenchymal transitionzh_TW
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.molonc.2014.12.009zh_TW
item.languageiso639-1en-
item.fulltextno fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
Appears in Collections:生物醫學研究所
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