Gene expression profile analysis of PLS-123 in xenograft model.
Ontology highlight
ABSTRACT: To exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in OCI-Ly7 inoculated xenograft model. Six- to eight-week-old male SCID mice were inoculated subcutaneously with OCI-Ly7 tumor cells in 0.1 ml PBS for tumor development
Project description:To exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in representative OCI-Ly7 cells treated for 48 hours. OCI-Ly7 cells were treated with ibrutinib, PLS-123 or vehicle for 48 hours.
Project description:To exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in OCI-Ly7 inoculated xenograft model.
Project description:To exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in representative OCI-Ly7 cells treated for 24 hours.
Project description:To provide insight into the role of and target genes of the transcription factor FOXP1 in mature human B cells and in B cell non-Hodkgin lymhomas, we performed gene expression microarray studies, upon ectopic overexpression or silencing of FOXP1 in these cells. human memory B cells from 2 separate donors were transduced with LZRS-FOXP1-IRES-YFP or LZRS-IRES-YFP (negative control); DLBCL cell lines OCI-Ly1, OCI-Ly7, and OCI-Ly10 were transduced with LZRS-FOXP1-IRES-YFP or LZRS-IRES-YFP (negative control); DLBCL cell lines OCI-Ly1, OCI-Ly7, and OCI-Ly10 were transiently transfected with siRNA targeting FOXP1 or sigenome non-targeting siRNA (negative control), using the Lonza nucleofection system.
Project description:The transcriptional repressors BCL6 and BACH2 are crucial regulators of germinal center (GC) B-cell fate, and are known to interact and repress transcription of PRDM1, a key driver of plasma cell differentiation. How these factors cooperate is not fully understood. Herein we show that while GC formation is only minimally impaired in Bcl6+/- or Bach2+/- mice, double heterozygous Bcl6+/-Bach2+/- mice exhibit profound reduction in GC formation. Splenic B-cells from Bcl6+/- Bach2+/- mice display accelerated plasmacytic differentiation and high expression of key plasma cell genes such as Prdm1, Xbp1 and CD138. ChIP-seq revealed that in B-cells BACH2 is mostly bound to genes together with its heterodimer partner MAFK. The BACH2-MAFK complex binds to sets of genes known to be involved in the GC response, 60% of which are also targets of BCL6. Approximately 30% of BACH2 peaks overlap with BCL6 including cis-regulatory sequences of the PRDM1 gene. BCL6 also modulates BACH2 protein stability and their protein levels are positively correlated in GC B-cells. Therefore, BCL6 and BACH2 cooperate to orchestrate gene expression patterning in GC B cells through both transcriptional and biochemical mechanisms, which collectively determine the proper initiation and timing of terminal differentiation. ChIP-seq using P18 antibodies in OCI-Ly7 cells