Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.20461
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dc.titleHypomethylation associated enhanced transcription of trefoil factor-3 mediates tamoxifen-stimulated oncogenicity of ER+ endometrial carcinoma cells
dc.contributor.authorPandey, V
dc.contributor.authorZhang, M
dc.contributor.authorChong, Q.-Y
dc.contributor.authorYou, M
dc.contributor.authorRaquib, A.R
dc.contributor.authorPandey, A.K
dc.contributor.authorLiu, D.-X
dc.contributor.authorLiu, L
dc.contributor.authorMa, L
dc.contributor.authorJha, S
dc.contributor.authorWu, Z.-S
dc.contributor.authorZhu, T
dc.contributor.authorLobie, P.E
dc.date.accessioned2020-09-01T00:57:55Z
dc.date.available2020-09-01T00:57:55Z
dc.date.issued2017
dc.identifier.citationPandey, V, Zhang, M, Chong, Q.-Y, You, M, Raquib, A.R, Pandey, A.K, Liu, D.-X, Liu, L, Ma, L, Jha, S, Wu, Z.-S, Zhu, T, Lobie, P.E (2017). Hypomethylation associated enhanced transcription of trefoil factor-3 mediates tamoxifen-stimulated oncogenicity of ER+ endometrial carcinoma cells. Oncotarget 8 (44) : 77268-77291. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.20461
dc.identifier.issn19492553
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/173802
dc.description.abstractTamoxifen (TAM) is widely used as an adjuvant therapy for women with breast cancer (BC). However, TAM possesses partial oestrogenic activity in the uterus and its use has been associated with an increased incidence of endometrial carcinoma (EC). The molecular mechanism for these observations is not well understood. Herein, we demonstrated that forced expression of Trefoil factor 3 (TFF3), in oestrogen receptorpositive (ER+) EC cells significantly increased cell cycle progression, cell survival, anchorage-independent growth, invasiveness and tumour growth in xenograft models. Clinically, elevated TFF3 protein expression was observed in EC compared with normal endometrial tissue, and its increased expression in EC was significantly associated with myometrial invasion. TAM exposure increased expression of TFF3 in ER+ EC cells and its elevated expression resulted in increased oncogenicity and invasiveness. TAM-stimulated expression of TFF3 in EC cells was associated with hypomethylation of the TFF3 promoter sequence and c-JUN/SP1-dependent transcriptional activation. In addition, small interfering (si) RNA-mediated depletion or polyclonal antibody inhibition of TFF3 significantly abrogated oncogenicity and invasiveness in EC cells consequent to TAM induction or forced expression of TFF3. Hence, TAM-stimulated upregulation of TFF3 in EC cells was critical in promoting EC progression associated with TAM treatment. Importantly, inhibition of TFF3 function might be an attractive molecular modality to abrogate the stimulatory effects of TAM on endometrial tissue and to limit the progression of EC. © Pandey et al.
dc.sourceUnpaywall 20200831
dc.subjectcaspase 7
dc.subjectcyclin D1
dc.subjectcyclin dependent kinase 2
dc.subjectcyclin dependent kinase 4
dc.subjectcyclin dependent kinase inhibitor 1B
dc.subjectestrogen receptor alpha
dc.subjectKi 67 antigen
dc.subjectmessenger RNA
dc.subjectprotein bcl 2
dc.subjectprotein c jun
dc.subjectprotein p53
dc.subjectscatter factor receptor
dc.subjectSTAT3 protein
dc.subjecttamoxifen
dc.subjecttranscription factor Snail
dc.subjecttranscription factor Sp1
dc.subjecttrefoil factor 3
dc.subjectTwist related protein 1
dc.subjectuvomorulin
dc.subjectadult
dc.subjectAN3-CA cell line
dc.subjectanchorage independent growth
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectapoptosis
dc.subjectArticle
dc.subjectBCL2 gene
dc.subjectBCL2L1 gene
dc.subjectcarcinogenicity
dc.subjectCASP7 gene
dc.subjectCCND1 gene
dc.subjectCCNE1 gene
dc.subjectCDK2 gene
dc.subjectCDK4 gene
dc.subjectCDKN1B gene
dc.subjectcell cycle progression
dc.subjectcell cycle S phase
dc.subjectcell migration
dc.subjectcell proliferation
dc.subjectcell survival
dc.subjectcell viability
dc.subjectclinical article
dc.subjectcohort analysis
dc.subjectcontrolled study
dc.subjectDNA methylation
dc.subjectECC-1 cell line
dc.subjectendometrial carcinoma cell line
dc.subjectendometrium
dc.subjectendometrium carcinoma
dc.subjectfemale
dc.subjectFN1 gene
dc.subjectgene expression regulation
dc.subjecthuman
dc.subjecthuman cell
dc.subjecthuman tissue
dc.subjectmarker gene
dc.subjectmouse
dc.subjectnonhuman
dc.subjectOCLN gene
dc.subjectpromoter region
dc.subjectprotein expression
dc.subjectRL95-2 cell line
dc.subjectTFF3 gene
dc.subjecttranscription initiation
dc.subjecttumor growth
dc.subjecttumor invasion
dc.subjecttumor suppressor gene
dc.subjecttumor volume
dc.subjecttumor xenograft
dc.subjectTWIST1 gene
dc.subjectupregulation
dc.subjectVIM gene
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentBIOCHEMISTRY
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.18632/oncotarget.20461
dc.description.sourcetitleOncotarget
dc.description.volume8
dc.description.issue44
dc.description.page77268-77291
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