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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 |
Appears in Collections: | Staff Publications |
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