Please use this identifier to cite or link to this item: https://doi.org/10.1210/en.2010-0273
Title: STAT3α is oncogenic for endometrial carcinoma cells and mediates the oncogenic effects of autocrine human growth hormone
Authors: Tang, J.-Z.
Kong, X.-J.
Banerjee, A.
Muniraj, N.
Pandey, V.
Steiner, M.
Perry, J.K.
Zhu, T.
Liu, D.-X.
Lobie, P.E. 
Issue Date: Sep-2010
Citation: Tang, J.-Z., Kong, X.-J., Banerjee, A., Muniraj, N., Pandey, V., Steiner, M., Perry, J.K., Zhu, T., Liu, D.-X., Lobie, P.E. (2010-09). STAT3α is oncogenic for endometrial carcinoma cells and mediates the oncogenic effects of autocrine human growth hormone. Endocrinology 151 (9) : 4133-4145. ScholarBank@NUS Repository. https://doi.org/10.1210/en.2010-0273
Abstract: We herein demonstrate an oncogenic role for signal transducer and activator of transcription (STAT)-3α (the full length STAT3 isoform), which also mediates autocrine human GH (hGH)-stimulated oncogenicity, in human endometrial carcinoma (EC) cells. Autocrine hGH stimulated Y705 phosphorylation of STAT3 and STAT3-mediated transcriptional activity in a SRC and Janus-2 Kinase dependent manner in human EC cell lines. Forced expression of a constitutively active variant of STAT3α increased proliferation, anchorage-independent, three-dimensional (3D) Matrigel, and xenograft growth and promoted epithelial-mesenchymal transition, migration, and invasion of EC cells. Conversely, the oncogenic capacity of EC cells was significantly impaired by treatment with JSI-124, an inhibitor of STAT3 phosphorylation and activity, small interfering RNA-mediated depletion of STAT3α, or a dominant-negative variant of STAT3α. Furthermore, the enhanced EC cell oncogenicity stimulated by autocrine hGH, was also abrogated by functional inhibition or small interfering RNA-mediated depletion of STAT3α. STAT3α may therefore be a common mediator of oncogenic signaling pathways stimulating progression of EC. Copyright © 2010 by The Endocrine Society.
Source Title: Endocrinology
URI: http://scholarbank.nus.edu.sg/handle/10635/110789
ISSN: 00137227
DOI: 10.1210/en.2010-0273
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