RANK-c attenuates aggressive properties of ER-negative breast cancer by inhibiting NF-κB activation and EGFR signaling

The RANK/RANKL axis emerges as a key regulator of breast cancer initiation, progression, and metastasis. RANK-c is a RANK receptor isoform produced through alternative splicing of the TNFRSF11A ( RANK ) gene and a dominant-negative regulator of RANK-induced nuclear factor-κB (NF-κB) activation. Here...

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Veröffentlicht in:	Oncogene 2018-09, Vol.37 (37), p.5101-5114
Hauptverfasser:	Sirinian, Chaido, Papanastasiou, Anastasios D., Schizas, Michail, Spella, Magda, Stathopoulos, Georgios T., Repanti, Maria, Zarkadis, Ioannis K., King, Tari A., Kalofonos, Haralabos P.
Format:	Artikel
Sprache:	eng
Schlagworte:	13/1 13/106 13/109 13/44 13/95 14/63 38/70 631/67/1347 631/67/1857 631/67/322 631/80/86/2368 82/29 82/80 96/21 96/31 96/35 Alternative splicing Animals Apoptosis Breast cancer Breast Neoplasms - metabolism Cell Biology Cell Line, Tumor Colonization Epidermal growth factor Epidermal growth factor receptors ErbB Receptors - metabolism Female Gene Expression Regulation, Neoplastic - physiology Genomes Human Genetics Humans Internal Medicine Kinases Medicine Medicine & Public Health Metastases Metastasis Mice Mice, Inbred NOD Mice, SCID NF-kappa B - metabolism NF-κB protein Oncology Osteoprotegerin Phosphorylation RANK Ligand - metabolism Receptor Activator of Nuclear Factor-kappa B - metabolism Receptors, Estrogen - metabolism Signal transduction Signal Transduction - physiology TRAF2 protein TRANCE protein Transcription Tumor cell lines Tumor necrosis factor receptors
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