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RNA-seq study on MLL-AF9 leukemia cells harboring JMJD1C sgRNAs targeting jumonji and zinc finger domains.

ABSTRACT: We transduced clonally MLL-AF9 leukemia cells expressing cas9 with sgRNA targeting the jumonji and zinc finger domains of JMJD1C. GFP (MLL-AF9) and TdTomato (sgRNA) double positive cells were sorted on Day 6 after transduction. Total RNA was isolated followed by mRNA selection. cDNA libraries were generated and NextGen Sequencing was performed.

ORGANISM(S): Mus musculus

PROVIDER: GSE129660 | GEO | 2019/04/12

REPOSITORIES: GEO

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Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia. To assess the effect of JMJD1C depletion on transcription, we compared the transcriptome of shJMJD1C- and shScr-transduced mouse MLL-AF9 transformed cells 48h after infection. A total of 451 transcripts were detected as changing between the two conditions (FDR<0.25)

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shRNA Screening Identifies JMJD1C as being required for Leukemia Maintenance (Agilent)

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