Signaling mechanisms of bortezomib in TRAF3-deficient mouse B lymphoma and human multiple myeloma cells

Highlights • Bortezomib induced Noxa and p21, and caused Mcl1 cleavage in TRAF3−/− tumor B cells. • Bortezomib exhibited contrasting roles on NF-κB1 and NF-κB2 pathways. • Oridonin or AD 198 drastically potentiated the anti-cancer effects of bortezomib.

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Leukemia research 2016-02, Vol.41, p.85-95
Hauptverfasser:	Edwards, Shanique K.E, Han, Yeming, Liu, Yingying, Kreider, Benjamin Z, Liu, Yan, Grewal, Sukhdeep, Desai, Anand, Baron, Jacqueline, Moore, Carissa R, Luo, Chang, Xie, Ping
Format:	Artikel
Sprache:	eng
Schlagworte:	AD 198 Animals Antineoplastic Agents - pharmacology B lymphoma Bortezomib Bortezomib - pharmacology Disease Models, Animal Hematology, Oncology and Palliative Medicine Humans Immunoblotting Immunoprecipitation Lymphoma, B-Cell - genetics Mice Multiple myeloma Multiple Myeloma - genetics Noxa Oridonin Proteasome Inhibitors - pharmacology Signal Transduction - drug effects TNF Receptor-Associated Factor 3 - deficiency TNF Receptor-Associated Factor 3 - genetics TRAF3 Transduction, Genetic
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Beschreibung
Zusammenfassung:	Highlights • Bortezomib induced Noxa and p21, and caused Mcl1 cleavage in TRAF3−/− tumor B cells. • Bortezomib exhibited contrasting roles on NF-κB1 and NF-κB2 pathways. • Oridonin or AD 198 drastically potentiated the anti-cancer effects of bortezomib.
ISSN:	0145-2126 1873-5835
DOI:	10.1016/j.leukres.2015.12.005