Please use this identifier to cite or link to this item: https://doi.org/10.1593/neo.10916
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dc.titleTrefoil factor 3 is oncogenic and mediates anti-estrogen resistance in human mammary carcinoma
dc.contributor.authorKannan, N.
dc.contributor.authorKang, I.
dc.contributor.authorKong, X.
dc.contributor.authorTang, J.
dc.contributor.authorPerry, J.K.
dc.contributor.authorMohankumar, K.M.
dc.contributor.authorMiller, L.D.
dc.contributor.authorLiu, E.T.
dc.contributor.authorMertani, H.C.
dc.contributor.authorZhu, T.
dc.contributor.authorGrandison, P.M.
dc.contributor.authorLiu, D.-X.
dc.contributor.authorLobie, P.E.
dc.date.accessioned2014-12-12T07:52:36Z
dc.date.available2014-12-12T07:52:36Z
dc.date.issued2010-12
dc.identifier.citationKannan, N., Kang, I., Kong, X., Tang, J., Perry, J.K., Mohankumar, K.M., Miller, L.D., Liu, E.T., Mertani, H.C., Zhu, T., Grandison, P.M., Liu, D.-X., Lobie, P.E. (2010-12). Trefoil factor 3 is oncogenic and mediates anti-estrogen resistance in human mammary carcinoma. Neoplasia 12 (12) : 1041-1053. ScholarBank@NUS Repository. https://doi.org/10.1593/neo.10916
dc.identifier.issn15228002
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/116661
dc.description.abstractWe report herein that trefoil factor 3 (TFF3) is oncogenic and mediates anti-estrogen resistance in human mammary carcinoma. Forced expression of TFF3 in mammary carcinoma cells increased cell proliferation and survival, enhanced anchorage-independent growth, and promoted migration and invasion. Moreover, forced expression of TFF3 increased tumor size in xenograft models. Conversely, depletion of endogenous TFF3 with small interfering RNA (siRNA) decreased the oncogenicity and invasiveness of mammary carcinoma cells. Neutralization of secreted TFF3 by antibody promoted apoptosis, decreased cell growth in vitro, and arrested mammary carcinoma xenograft growth. TFF3 expression was significantly correlated to decreased survival of estrogen receptor (ER)-positive breast cancer patients treated with tamoxifen. Forced expression of TFF3 in mammary carcinoma cells increased ER transcriptional activity, promoted estrogen-independent growth, and produced resistance to tamoxifen and fulvestrant in vitro and to tamoxifen in xenograft models. siRNA-mediated depletion or antibody inhibition of TFF3 significantly enhanced the efficacy of antiestrogens. Increased TFF3 expression was observed in tamoxifen-resistant (TAMR) cells and antibody inhibition of TFF3 in TAMR cells improved tamoxifen sensitivity. Functional antagonism of TFF3 therefore warrants consideration as a novel therapeutic strategy for mammary carcinoma. © 2010 Neoplasia Press, Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1593/neo.10916
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1593/neo.10916
dc.description.sourcetitleNeoplasia
dc.description.volume12
dc.description.issue12
dc.description.page1041-1053
dc.description.codenNEOPF
dc.identifier.isiut000285209400009
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