Abstract
Glucocorticoids (GCs) induce cell cycle arrest and apoptosis in lymphoid cells and constitute a central component in the treatment of lymphoid malignancies. The molecular basis of this clinically important phenomenon remains, however, poorly understood. Using whole genome expression profiling we have previously identified glucocorticoid response genes in children with acute lymphoblastic leukemia (ALL). The promyelocytic leukemia zinc finger (PLZF) appeared as one of the most promising candidate genes, which has been implicated in the pathogenesis of several leukemia types. We have already established that transgenic PLZF reduced the sensitivity to GC-induced apoptosis in the CEM-C7H2-2C8 leukemic cell line and knockdown of PLZF resulted in a small but significant increase in cell death in this cell line. The present study was proposed to find a plausible molecular explanation for this protective effect of PLZF against GC-induced cell death. It was found that doxycycline-regulated PLZF overexpression in the CCRF- CEM T-ALL cell line downregulates the GC-induced GR expression and its target genes, which resulted in reduced apoptosis induced by GC.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
