Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/81297
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dc.contributorDepartment of Biomedical Engineering-
dc.creatorChen, JJ-
dc.creatorXiao, ZJ-
dc.creatorMeng, XJ-
dc.creatorWang, Y-
dc.creatorYu, MK-
dc.creatorHuang, WQ-
dc.creatorSun, X-
dc.creatorChen, H-
dc.creatorDuan, YG-
dc.creatorJiang, XH-
dc.creatorWong, MP-
dc.creatorChan, HC-
dc.creatorZou, F-
dc.creatorRuan, YC-
dc.date.accessioned2019-09-20T00:54:57Z-
dc.date.available2019-09-20T00:54:57Z-
dc.identifier.urihttp://hdl.handle.net/10397/81297-
dc.language.isoenen_US
dc.publisherIvyspring International Publisheren_US
dc.rights© The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.en_US
dc.rightsThe following publication Chen JJ, Xiao ZJ, Meng X, Wang Y, Yu MK, Huang WQ, Sun X, Chen H, Duan YG, Jiang X, Wong MP, Chan HC, Zou F, Ruan YC. MRP4 sustains Wnt/β-catenin signaling for pregnancy, endometriosis and endometrial cancer. Theranostics 2019; 9(17):5049-5064 is available at https://dx.doi.org/10.7150/thno.32097en_US
dc.subjectMRP4en_US
dc.subjectWnt/beta-cateninen_US
dc.subjectEndometriumen_US
dc.subjectEmbryo implantationen_US
dc.subjectEndometriosisen_US
dc.subjectEndometrial canceren_US
dc.titleMRP4 sustains Wnt/beta-catenin signaling for pregnancy, endometriosis and endometrial canceren_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage5049-
dc.identifier.epage5064-
dc.identifier.volume9-
dc.identifier.issue17-
dc.identifier.doi10.7150/thno.32097-
dcterms.abstractRationale: Abnormal Wnt/beta-catenin signaling in the endometrium can lead to both embryo implantation failure and severe pathogenic changes of the endometrium such as endometrial cancer and endometriosis. However, how Wnt/beta-catenin signaling is regulated in the endometrium remains elusive. We explored possible regulation of Wnt/beta-catenin signaling by multi-drug resistance protein 4 (MRP4), a potential target in cancer chemotherapy, and investigated the mechanism.-
dcterms.abstractMethods: Knockdown of MRP4 was performed in human endometrial cells in vitro or in a mouse embryo-implantation model in vivo. Immunoprecipitation, immunoblotting and immunofluorescence were used to assess protein interaction and stability. Wnt/beta-catenin signaling was assessed by TOPflash reporter assay and quantitative PCR array. Normal and endometriotic human endometrial tissues were examined. Data from human microarray or RNAseq databases of more than 100 participants with endometriosis, endometrial cancer or IVF were analyzed. In vitro and in vivo tumorigenesis was performed.-
dcterms.abstractResults: MRP4-knockdown, but not its transporter-function-inhibition, accelerates beta-catenin degradation in human endometrial cells. MRP4 and beta-catenin are co-localized and co-immunoprecipitated in mouse and human endometrium. MRP4-knockdown in mouse uterus reduces beta-catenin levels, downregulates a series of Wnt/beta-catenin target genes and impairs embryo implantation, which are all reversed by blocking beta-catenin degradation. Analysis of human endometrial biopsy samples and available databases reveals significant and positive correlations of MRP4 with beta-catenin and Wnt/beta-catenin target genes in the receptive endometrium in IVF, ectopic endometriotic lesions and endometrial cancers. Knockdown of MRP4 also inhibits in vitro and in vivo endometrial tumorigenesis.-
dcterms.abstractConclusion: A previously undefined role of MRP4 in stabilizing beta-catenin to sustain Wnt/beta-catenin signaling in endometrial cells is revealed for both embryo implantation and endometrial disorders, suggesting MRP4 as a theranostic target for endometrial diseases associated with Wnt/beta-catenin signaling abnormality.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationTheranostics, 2019, v. 9, no. 17, p. 5049-5064-
dcterms.isPartOfTheranostics-
dcterms.issued2019-
dc.identifier.isiWOS:000474898900017-
dc.identifier.scopus2-s2.0-85070483866-
dc.identifier.eissn1838-7640-
dc.description.validate201909 bcrc-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_Scopus/WOSen_US
dc.description.pubStatusPublisheden_US
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