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ShRNA-mediated Myc knockdown and shRNA-mediated knockdown of Myc-induced lncRNA KTN1-AS1 in ST486 Burkitt lymphoma cells

ABSTRACT: shRNA-mediated Myc knockdown and shRNA-mediated knockdown of Myc-induced lncRNA KTN1-AS1 in ST486 Burkitt lymphoma cells

PROVIDER: PRJNA490714 | ENA |

REPOSITORIES: ENA

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Gene expression analysis after shRNA-mediated knockdown of Myc-induced lncRNA KTN1-AS1 in ST486 Burkitt lymphoma cells

Project description:Gene expression analysis after shRNA-mediated knockdown of Myc-induced lncRNA KTN1-AS1 in ST486 Burkitt lymphoma cells

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Expression analysis of mRNA and lncRNA expression levels after shRNA-mediated Myc knockdown in ST486 Burkitt lymphoma cells

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Expression profiling of Burkitt's lymphoma cells 24h after FOXM1 shRNA or MYB shRNA lentivirus-mediated transduction

Project description:Human Burkitt's lymphoma ST486 cells were transduced with non-target control shRNA lentiviral vectors, FOXM1 shRNA, and MYB shRNA lentiviral vectors. Total RNA was isolated 24h later. cRNA was produced with the standard one-step IVT protocol (Affymetix) and hybridized in U95Av2 gene chips (Affymetrix). Experiment consists in 3 independent samples: Expression profiling of Burkitt's lymphoma cells 24h after non-target control shRNA lentiviral mediated transduction. Expression profiling of Burkitt's lymphoma cells 24h after FOXM1 shRNA lentiviral mediated transduction. Expression profiling of Burkitt's lymphoma cells 24h after MYB shRNA lentiviral mediated transduction. Data processing performed using MAS5 or GCRMA.

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Gene expression analysis after shRNA-mediated knockdown of Myc-induced lncRNA KTN1-AS1 in ST486 Burkitt lymphoma cells

Project description:The oncogenic transcription factor (c-)Myc is overexpressed in a variety of cancers including subtypes of B cell lymphoma. Here we study long noncoding (lnc)RNAs regulated by Myc, arguing that these lncRNAs may be involved in the very strong effect of Myc on cell proliferation. Using multiple in vitro models and taking into account the kinetics of the response to Myc as well as Myc binding sites we defined two Myc-induced and four Myc-repressed lncRNA candidates. Expression levels of the top Myc-induced lncRNA KTN1-AS1 are low in normal B cell subsets and strongly increased in multiple Myc-positive lymphoma cell lines. In addition, primary lymphoma cases stratified by high or low Myc expression show the expected KTN1-AS1 expression differences. Knockdown of KTN1-AS1 severely impaired the cell growth of multiple Burkitt lymphoma cell lines. Gene expression analysis showed that KTN1-AS1 knockdown affects >300 genes genome wide with a strong enrichment of Myc-target genes involved in metabolism and biosynthesis. In line with this finding, KTN1-AS1 depletion in B cell lymphoma cells caused a substantial decrease of Myc transcript and protein. Thus, our data indicates that KTN1-AS1 overexpression in lymphoma may reinforce high Myc expression at the transcriptional level to activate gene expression programs supporting the high metabolic rate present in lymphoma cells. In conclusion, we identified a novel positive feedback loop between c-Myc and KTN1-AS1 in B cell lymphoma cells. LncRNAs such as KTN1-AS1, that regulate important oncogenic factors in specific cell types, may open new ways to cancer therapy.

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