IL-32θ inhibits stemness and epithelial-mesenchymal transition of cancer stem cells via the STAT3 pathway in colon cancer

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dc.contributor.authorY Bak-
dc.contributor.authorTaeho Kwon-
dc.contributor.authorIn Seon Bak-
dc.contributor.authorJ Hong-
dc.contributor.authorDae Yeul Yu-
dc.contributor.authorD Y Yoon-
dc.date.accessioned2017-04-19T10:18:45Z-
dc.date.available2017-04-19T10:18:45Z-
dc.date.issued2016-
dc.identifier.issn19492553-
dc.identifier.uri10.18632/oncotarget.7007ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13164-
dc.description.abstractInterleukin (IL)-32 is a well-known cytokine associated with inflammation, virus infections and cancer. IL-32θ is a newly identified isoform of IL-32, whose function has yet to be elucidated. In this study, we investigated IL-32θ function in colon cancer stem cells. Using samples from colon cancer patients, we found that the expression of IL-32θ mRNAs was significantly suppressed in tumor regions. We investigated the effects of IL-32θ on colon cancer. Ectopic expression of IL-32θ attenuated invasion, migration in vitro and in vivo tumorigenicity of colon cancer cells. IL-32θ inhibited epithelial-mesenchymal transition (EMT), resulting in the suppression of their migratory and invasive capabilities of HT29 colon cancer cells. In addition, IL-32θ altered various properties of CSCs, including sphere formation and expression of stemness related genes. IL-32θ directly bound to STAT3 and inhibited its nuclear translocation, leading to inhibited transcription of downstream factors, including Bmi1 and ZEB1. We showed that IL-32θ inhibited the STAT3-ZEB1 pathway and consequently inhibited key factors of stemness and EMT. Taken together, our findings reveal that IL-32θ can be a tumor suppressor, indicating that IL-32θ could possibly be used in therapies for colon cancer.-
dc.publisherImpact Journalsko
dc.titleIL-32θ inhibits stemness and epithelial-mesenchymal transition of cancer stem cells via the STAT3 pathway in colon cancer-
dc.title.alternativeIL-32θ inhibits stemness and epithelial-mesenchymal transition of cancer stem cells via the STAT3 pathway in colon cancer-
dc.typeArticle-
dc.citation.titleOncotarget-
dc.citation.number6-
dc.citation.endPage7317-
dc.citation.startPage7307-
dc.citation.volume7-
dc.contributor.affiliatedAuthorTaeho Kwon-
dc.contributor.alternativeName박예솔-
dc.contributor.alternativeName권태호-
dc.contributor.alternativeName박인선-
dc.contributor.alternativeName홍진태-
dc.contributor.alternativeName유대열-
dc.contributor.alternativeName윤도영-
dc.identifier.bibliographicCitationOncotarget, vol. 7, no. 6, pp. 7307-7317-
dc.identifier.doi10.18632/oncotarget.7007-
dc.subject.keywordCancer stem cells-
dc.subject.keywordColon cancer-
dc.subject.keywordEMT-
dc.subject.keywordIL-32-
dc.subject.keywordStemness-
dc.subject.localCancer stem cells-
dc.subject.localCancer stem cell-
dc.subject.localColon cancer-
dc.subject.localEMT-
dc.subject.localIL-32-
dc.subject.localStemness-
dc.description.journalClassN-
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Jeonbuk Branch Institute > Primate Resources Center > 1. Journal Articles
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