Suppression Of Cdc37 Induces Btz Resistance Through Xbp1s Mediated Plasma Cell Immaturation In Multiple Myeloma

Backgrounds: Cell division cycle protein 37 (Cdc37) is considered as a key co-chaperone of heat shock protein 90 (Hsp90), guiding the stabilization and activation of client kinases with time specificity and substrate selectivity. Previous studies have demonstrated that Cdc37 is over-expressed in many kinds of cancers, contributing to the tumorigenesis. However, our previous study suggested that some MM cell population with low expression of Cdc37 was correlated with BTZ resistance in clinical MM samples and in vitro study. The purpose of this study is to investigate how Cdc37 contributes to drug resistance in MM.