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dc.contributor.authorZhao, Y.en_US
dc.contributor.authorYang, Y.en_US
dc.contributor.authorTrovik, Joneen_US
dc.contributor.authorSun, Kunen_US
dc.contributor.authorZhou, Liangen_US
dc.contributor.authorJiang, Peiyongen_US
dc.contributor.authorLau, Tatsanen_US
dc.contributor.authorHøivik, Erling Andreen_US
dc.contributor.authorSalvesen, Helgaen_US
dc.contributor.authorSun, H.en_US
dc.contributor.authorWang, H.en_US
dc.date.accessioned2020-06-16T09:06:53Z
dc.date.available2020-06-16T09:06:53Z
dc.date.issued2019
dc.PublishedZhao Y, Yang Y, Trovik J, Sun K, Zhou L, Jiang P, Lau, Høivik EA, Salvesen H, Sun, Wang H. Novel PCDH10-Wnt-MALAT1 regulatory axis in endometrioid endometrial adenocarcinoma. Hong Kong Medical Journal. 2019;25(5):17-22eng
dc.identifier.issn2226-8707
dc.identifier.issn1024-2708
dc.identifier.urihttps://hdl.handle.net/1956/22619
dc.description.abstractKey Messages: 1. Protocadherin 10 (PCDH10) is silenced in endometrioid endometrial cancer through promoter hypermethylation. 2. Ectopic expression of PCDH10 inhibits tumour growth and induces cell apoptosis. 3. Transcriptomic analysis revealed that PCDH10 expression down-regulates metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). Further mechanistic studies uncovered that MALAT1 expression is transcriptionally induced by Wnt/β-catenin signalling. 4. We uncovered a novel PCDH10-Wnt/β-cateninMALAT1 regulatory axis that contributes to development and progression of endometrioid endometrial cancer.en_US
dc.language.isoengeng
dc.publisherHong Kong Academy of Medicineeng
dc.rightsAttribution-NonCommercial-NoDerivatives CC BY-NC-ND 4.0eng
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/eng
dc.titleNovel PCDH10-Wnt-MALAT1 regulatory axis in endometrioid endometrial adenocarcinomaen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2020-02-08T10:17:23Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2019 The Hong Kong Medical Journal
dc.identifier.cristin1788058
dc.source.journalHong Kong Medical Journal


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Attribution-NonCommercial-NoDerivatives CC BY-NC-ND 4.0
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