MRNA prolfiles of subcutaneous SK-N-BE(2) xenografts treated with the KIF11 inhibitor 4SC-205
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PROVIDER: PRJNA702520 | ENA |
REPOSITORIES: ENA
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Project description:The aim of these study is to investiate the expression profile of neuroblastoma SK-N-BE(2) xenografts treated with one single dose of the KIF11 inhibitor 4SC-205 for 24 h. RNASeq libraries were prepared following the TruSeq® Stranded mRNA LT Sample Prep Kit protocol and sequenced on NovaSeq 6000 (Illumina). RNA-seq reads were mapped against human reference genome (GRCh38) using STAR software version 2.5.3a with ENCODE parameters. Genes were quantified using RSEM version 1.3.0. Tumors treated with 4SC-205 presented increased expression of genes involved in the G2/M checkpoint and E2F targets. Genes of mTORC1 pathway were found to be less expressed on treated tumors otherwise. This study demonstrates that KIF11 inhibition using 4SC-205 halts cell cycle progression of cancerous cells of neuroblastoma xenografts.
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Project description:Development of model systems that recapitulate the molecular heterogeneity observed amongst GBM tumors will expedite the testing of targeted molecular therapeutic strategies for GBM treatment. In this study, we profiled DNA copy number and mRNA expression in 21 independent GBM tumor lines maintained as subcutaneous xenografts (GBMX), and compared GBMX molecular signatures to those observed in GBM clinical specimens derived from The Cancer Genome Atlas (TCGA). The predominant copy number signature in both tumor groups was defined by chromosome-7-gain/chromosome-10-loss, a poor prognosis genetic signature. We also observed, at frequencies similar to that detected in TCGA GBMs genomic amplification and overexpression of known GBM oncogenes such as EGFR, MDM2, CDK6 and MYCN, and novel genes including NUP107, SLC35E3, MMP1, MMP13 and DDX1. The transcriptional signature of GBMX tumors, which was stable over multiple subcutaneous passages, was defined by overexpression of genes involved in M-phase, DNA Replication, and Chromosome organization (MRC) and was highly similar to the poor-prognosis mitosis-and-cell-cycle-module (MCM) in GBM. Assessment of gene expression in TCGA-derived GBMs revealed overexpression of MRC cancer genes AURKB, BIRC5, CCNB1, CCNB2, CDC2, CDK2, and FOXM1, which form a transcriptional network important for G2/M- progression and/or -checkpoint activation. In conclusion, our study supports propagation of GBM tumors as subcutaneous xenografts as a useful approach for sustaining key molecular characteristics of patient tumors, and highlights therapeutic opportunities conferred by this GBMX tumor panel for testing targeted therapeutic strategies for GBM treatment. Keywords: Disease state analysis
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