XPO1 (CRM1) inhibition represses STAT3 activation to drive a survivin-dependent oncogenic switch in triple-negative breast cancer

Inhibition of XPO1 (CRM1)-mediated nuclear export of multiple tumor suppressor proteins has been proposed as a novel cancer therapeutic strategy to turn off oncogenic signals and enhance tumor suppression. Survivin is a multifunctional protein with oncogenic properties when expressed in the cytoplas...

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Veröffentlicht in:	Molecular cancer therapeutics 2014-03, Vol.13 (3), p.675-686
Hauptverfasser:	Cheng, Yan, Holloway, Michael P, Nguyen, Kevin, McCauley, Dilara, Landesman, Yosef, Kauffman, Michael G, Shacham, Sharon, Altura, Rachel A
Format:	Artikel
Sprache:	eng
Schlagworte:	Active Transport, Cell Nucleus - genetics Apoptosis - drug effects Caspase 3 Cell Line, Tumor Cell Nucleus - genetics Cell Nucleus - metabolism Exportin 1 Protein Female Genetic Therapy Humans Inhibitor of Apoptosis Proteins - genetics Karyopherins - antagonists & inhibitors Karyopherins - genetics Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors Receptors, Cytoplasmic and Nuclear - genetics STAT3 Transcription Factor - genetics Survivin Triple Negative Breast Neoplasms - genetics Triple Negative Breast Neoplasms - pathology Triple Negative Breast Neoplasms - therapy
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