Please use this identifier to cite or link to this item: https://doi.org/10.1158/0008-5472.CAN-10-2787
Title: FOXQ1 regulates epithelial-mesenchymal transition in human cancers
Authors: Qiao, Y.
Jiang, X.
Lee, S.T.
Karuturi, R.K.M.
Hooi, S.C.
Yu, Q. 
Issue Date: 15-Apr-2011
Citation: Qiao, Y., Jiang, X., Lee, S.T., Karuturi, R.K.M., Hooi, S.C., Yu, Q. (2011-04-15). FOXQ1 regulates epithelial-mesenchymal transition in human cancers. Cancer Research 71 (8) : 3076-3086. ScholarBank@NUS Repository. https://doi.org/10.1158/0008-5472.CAN-10-2787
Abstract: Epithelial-mesenchymal transition (EMT) in cancer cells plays a pivotal role in determining metastatic prowess, but knowledge of EMT regulation remains incomplete. In this study, we defined a critical functional role for the Forkhead transcription factor FOXQ1 in regulating EMT in breast cancer cells. FOXQ1 expression was correlated with high-grade basal-like breast cancers and was associated with poor clinical outcomes. RNAimediated suppression of FOXQ1 expression in highly invasive human breast cancer cells reversed EMT, reduced invasive ability, and alleviated other aggressive cancer phenotypes manifested in 3-dimensional Matrigel (BD Biosciences) culture. Conversely, enforced expression of FOXQ1 in differentiated human mammary epithelial cells (HMLER) or epithelial cancer cell lines provoked an epithelial to mesenchymal morphologic change, gain of stem cell-like properties, and acquisition of resistance to chemotherapy-induced apoptosis. Mechanistic investigations revealed that FOXQ1-induced EMT was associated with transcriptional inactivation of the epithelial regulator E-cadherin (CDH1). Our findings define a key role for FOXQ1 in regulating EMT and aggressiveness in human cancer. © 2011 American Association for Cancer Research.
Source Title: Cancer Research
URI: http://scholarbank.nus.edu.sg/handle/10635/113216
ISSN: 00085472
DOI: 10.1158/0008-5472.CAN-10-2787
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