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Article: The Wnt modulator ICG‑001 mediates the inhibition of nasopharyngeal carcinoma cell migration in vitro via the miR‑150/CD44 axis

TitleThe Wnt modulator ICG‑001 mediates the inhibition of nasopharyngeal carcinoma cell migration in vitro via the miR‑150/CD44 axis
Authors
Keywords3' untranslated region
animal experiment
animal model
animal tissue
antigen expression
Issue Date2018
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/
Citation
International Journal of Oncology, 2018, v. 54 n. 3, p. 1010-1020 How to Cite?
AbstractThe Wnt signaling pathway is known to serve an important role in the control of cell migration. The present study analyzed the mechanisms underlying the in vitro modulation of the migration of nasopharyngeal carcinoma (NPC) cells by the CREB‑binding protein/catenin antagonist and Wnt modulator ICG‑001. The results revealed that ICG‑001‑mediated inhibition of tumor cell migration involved downregulated mRNA and protein expression of the Wnt target gene cluster of differentiation (CD)44. It was also demonstrated that ICG‑001 downregulated the expression of CD44, and this effect was accompanied by restored expression of microRNA (miRNA)‑150 in various NPC cell lines. Using a CD44 3'‑untranslated region luciferase reporter assay, miR‑150 was confirmed to be a novel CD44‑targeting miRNA, which could directly target CD44 and subsequently regulate the migration of NPC cells. The present study provides further insight into the inhibition of tumor cell migration through the modulation of miRNA expression by the Wnt modulator ICG‑001.
Persistent Identifierhttp://hdl.handle.net/10722/272154
ISSN
2017 Impact Factor: 3.333
2015 SCImago Journal Rankings: 1.270

 

DC FieldValueLanguage
dc.contributor.authorChan, LS-
dc.contributor.authorMan, OY-
dc.contributor.authorKwok, HH-
dc.contributor.authorChen, L-
dc.contributor.authorChan, KC-
dc.contributor.authorLung, HL-
dc.contributor.authorNgan, RKC-
dc.contributor.authorWong, RNS-
dc.contributor.authorLo, KW-
dc.contributor.authorLee, AWM-
dc.contributor.authorTsao, GSW-
dc.contributor.authorKahn, M-
dc.contributor.authorLung, ML-
dc.contributor.authorMak, NK-
dc.date.accessioned2019-07-20T10:36:43Z-
dc.date.available2019-07-20T10:36:43Z-
dc.date.issued2018-
dc.identifier.citationInternational Journal of Oncology, 2018, v. 54 n. 3, p. 1010-1020-
dc.identifier.issn1019-6439-
dc.identifier.urihttp://hdl.handle.net/10722/272154-
dc.description.abstractThe Wnt signaling pathway is known to serve an important role in the control of cell migration. The present study analyzed the mechanisms underlying the in vitro modulation of the migration of nasopharyngeal carcinoma (NPC) cells by the CREB‑binding protein/catenin antagonist and Wnt modulator ICG‑001. The results revealed that ICG‑001‑mediated inhibition of tumor cell migration involved downregulated mRNA and protein expression of the Wnt target gene cluster of differentiation (CD)44. It was also demonstrated that ICG‑001 downregulated the expression of CD44, and this effect was accompanied by restored expression of microRNA (miRNA)‑150 in various NPC cell lines. Using a CD44 3'‑untranslated region luciferase reporter assay, miR‑150 was confirmed to be a novel CD44‑targeting miRNA, which could directly target CD44 and subsequently regulate the migration of NPC cells. The present study provides further insight into the inhibition of tumor cell migration through the modulation of miRNA expression by the Wnt modulator ICG‑001.-
dc.languageeng-
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/-
dc.relation.ispartofInternational Journal of Oncology-
dc.subject3' untranslated region-
dc.subjectanimal experiment-
dc.subjectanimal model-
dc.subjectanimal tissue-
dc.subjectantigen expression-
dc.titleThe Wnt modulator ICG‑001 mediates the inhibition of nasopharyngeal carcinoma cell migration in vitro via the miR‑150/CD44 axis-
dc.typeArticle-
dc.identifier.emailChan, KC: biocandy@hku.hk-
dc.identifier.emailLung, HL: hllung2@hku.hk-
dc.identifier.emailNgan, RKC: rkcngan@hku.hk-
dc.identifier.emailLee, AWM: awmlee@hkucc.hku.hk-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailLung, ML: mlilung@hku.hk-
dc.identifier.authorityLung, HL=rp00299-
dc.identifier.authorityNgan, RKC=rp02371-
dc.identifier.authorityLee, AWM=rp02056-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityLung, ML=rp00300-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3892/ijo.2018.4664-
dc.identifier.pmid30569106-
dc.identifier.scopuseid_2-s2.0-85060625200-
dc.identifier.hkuros299025-
dc.identifier.volume54-
dc.identifier.issue3-
dc.identifier.spage1010-
dc.identifier.epage1020-
dc.publisher.placeGreece-

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