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PCALCL cell line Mac1:vehicle control vs.shEZH2

ABSTRACT: Transcriptional profiling of human PCALCL cell line Mac1 comparing cells transfected with vehicle control with shEZH2 cells. Previous study have shown the involvements of EZH2 in T cell development and hematopoietic malignancies of T-cell origin. Objective was to explore the action of EZH2 in the pathogenesis of cutaneous T-cell lymphoma(CTCL).

ORGANISM(S): Homo sapiens

PROVIDER: GSE96742 | GEO | 2018/03/31

REPOSITORIES: GEO

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CTCL cell line H9:vehicle control vs.ShBCL11B

Project description:Transcriptional profiling of human CTCL cell line H9 comparing cells transfected with vehicle control with ShBCL11B cells. Previous study have shown the involvements of BCL11b/BCL11B in T cell development and hematopoietic malignancies of T-cell origin. Objective was to explore the action of BCL11B in the pathogenesis of cutaneous T-cell lymphoma(CTCL).

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Project description:Developing targeted therapy for cutaneous T cell lymphoma (CTCL) patients still requires actionable mutated genes and deregulated pathways to be identified. There is increasing evidence that activating mutations in JAK genes and deregulated JAK/STAT signaling are important mechanisms involved in multiple B and T cell malignancies, including CTCL. Therefore, in this study we focused on studying the mutational status of JAK1, JAK2 and JAK3 genes in a series of human CTCL lesions and cell lines using next-generation sequencing (NGS). We found that 7 of 48 (14.7%) of the analyzed cases harbored mutations in the JAK1 and JAK3 genes that mainly affected the pseudokinase domain of the corresponding proteins. On the basis of these results, we used a specific JAK inhibitor (INCB018424) in a series of CTCL cell lines with deregulated JAK/STAT activity. Treatment of CTCL cells with INCB018424 resulted in dose-dependent reduction of activated STAT expression, diminished cell viability, and increased apoptosis. We also studied global changes in gene expression in cells with mutated JAK1 and JAK3 proteins treated with INCB018424 and identified multiple genes that were differentially regulated by JAK/STAT signaling, such as FGF20 (upregulated) and EGR1 (downregulated). Thus, our results show that the detection of deregulated JAK/STAT signaling in CTCL lesions via JAK mutations or other surrogate markers may serve to indicate the clinical use of JAK/STAT inhibitors. 3 replicates of cells treated with DMSO or JAKi during 30 min and 3h

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