Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Inhibition of miR-9 regulates HuR and DICER1 and blocks Hodgkin Lymphoma tumor outgrowth

ABSTRACT: An Hodgkin Lymphoma cell line have been treated with an LNA inhibitor for miR-9 or with a scramble LNA to identify miR-9 regulated pathways that could be important for Hodgkin Lymphoma pathogenesis. L428 cells were transfected with a miR-9 LNA inhibitor or a scrambled LNA. Total RNA was harvested 9 hours post-transfection and analyzed on Affymetrix HG-U133 Plus 2.0 human arrays. A total of six arrays were analyzed. For filtering, uninformative genes with the same expression level across all arrays (including non-expressed genes) were removed and the differentially expressed genes, their corresponding p-values and false discovery rates were calculated using limma.

ORGANISM(S): Homo sapiens

SUBMITTER: Lea Gregersen

PROVIDER: E-GEOD-27529 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Inhibition of miR-9 de-represses HuR and DICER1 and impairs Hodgkin lymphoma tumour outgrowth in vivo.

Leucci E E Zriwil A A Gregersen L H LH Jensen K T KT Obad S S Bellan C C Leoncini L L Kauppinen S S Lund A H AH

Oncogene 20120206 49

MicroRNAs are important regulators of gene expression in normal development and disease. miR-9 is overexpressed in several cancer forms, including brain tumours, hepatocellular carcinomas, breast cancer and Hodgkin lymphoma (HL). Here we demonstrated a relevance for miR-9 in HL pathogenesis and identified two new targets Dicer1 and HuR. HL is characterized by a massive infiltration of immune cells and fibroblasts in the tumour, whereas malignant cells represent only 1% of the tumour mass. These ...[more]

PMID: 22310293

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Project description:We examined the biological effects of a potent second-generation proteasome inhibitor, ixazomib, in T-cell lymphoma and Hodgkin lymphoma cell lines and human xenograft models. Ixazomib resulted in time- and dose-dependent cytotoxicity and apoptosis in all cell lines (IC50’s <75nM). In vivo studies via SCID tumor xenografts showed significant inhibition of tumor growth (P<0.001) with significantly improved survival (P<0.001) in Jurkat and L540 models with ixazomib-treated mice versus controls. Through global transcriptome and network analyses, ixazomib-treated Jurkat and L540 cells showed significant overlap in biological functions involved in regulation of cell cycle, chromatin modification, and DNA repair processes with a lack of conservation observed in a relatively ixazomib-resistant cell line, L428. Moreover, the predicted activation and inhibition status of tumor suppressors and oncogenes strongly favored ixazomib inhibition of tumor progression. Most notably, ixazomib down-regulated protein levels of MYC and its target genes. Additionally, chromatin immunoprecipitation showed that histone H3 acetylation affected MYC levels and cell death response to ixazomib. Furthermore, inhibition of MYC with JQ1 resulted in synergistic cell death in L428, which was confirmed utilizing MYC knockout. Collectively, ixazomib down-regulated MYC and downstream substrates in TCL and HL, while resistance appeared mediated through MYC- and CHK1-dependent mechanisms. L428 cells were treated with 25nM ixazomib for 24 hours, RNA was isolated using RNeasy Minikit (Qiagen), following instructions recommended supplied by the manufacturer. Purity and the yield of isolated RNA was determined using Bioanalyzer. These experiments were performed in biological triplicates. Microarray experiment with L428 was performed using Human HT 12 Genechip Illumina. Data for the L428 cell line was corrected through normalization of the housekeeping genes, quantile normalized, and then statistically relevant genes were determined with one-way ANOVA analysis with FDR <0.05.

Dataset Information

Inhibition of miR-9 regulates HuR and DICER1 and blocks Hodgkin Lymphoma tumor outgrowth

Publications

Inhibition of miR-9 de-represses HuR and DICER1 and impairs Hodgkin lymphoma tumour outgrowth in vivo.

Similar Datasets

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