Bulk sequencing of MYCN-overexpressing chicken retinal cell lines
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ABSTRACT:
PROVIDER: PRJNA818671 | ENA |
REPOSITORIES: ENA
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Project description:Background: MYCN gene is a transcription factor whose amplification and overexpression can lead to tumorigenesis. In retina, MYCN overexpression is related to tumorigenesis of retinoblastoma, a childhood cancer. Purpose: To find out differentially expressed genes in MYCN-overexpressing cells, which will give information of MYCN-related gene expression and possibly find out new pathways in mechanism of retinoblastoma tumorigenesis with MYCN overexpression. Methods: MYCN-overexpressing cells were taken from MYCN electroporated E14 chicken retina and kept in culture for over 4 weeks. Unelectroporated E14 chicken retina central region was dissected as a control. Total RNA was extracted and sequenced on Illumina NovaSeq 6000. The data were used for differential expression analysis and GO/Pathway enrichment analysis. Results: Genes related to proliferation were upregulated in MYCN-overexpressing cells, while genes related to neural differentiation were downregulated. GO/Pathway enrichment analysis showed that upregulated genes were enriched for pathways associated with cell proliferation and downregulated genes for neural differentiation.
2022-06-30 | GSE199162 | GEO
Project description:Background: MYCN gene is a transcription factor whose amplification and overexpression can lead to tumorigenesis. In retina, MYCN overexpression is related to tumorigenesis of retinoblastoma, a childhood cancer. Purpose: To find out differentially expressed genes in MYCN-overexpressing cells, which will give information of MYCN-related gene expression and possibly find out new pathways in mechanism of retinoblastoma tumorigenesis with MYCN overexpression. Methods: MYCN-overexpressing cells were taken from MYCN electroporated E14 chicken retina and kept in culture. Unelectroporated E14 chicken retina central region was dissected as a control. Total RNA was extracted and sequenced on Illumina NovaSeq 6000. The data were used for differential expression analysis and GO/Pathway enrichment analysis.
2024-03-11 | GSE226458 | GEO
Project description:RNA-seq upon MYCN activation in the hTERT-immortalized MYCN retinal pigmented epithelial cell line (RPE1–MYCN-ER). The parental hTERT-immortalized retinal pigment epithelium (hTERT-RPE1) was used as a control as this cell line does not carry the MYCN:ER expression construct. Both cell lines were treated with tamoxifen (400nM; 4-OHT) for MYCN induction (with 4-OHT or not). Analysis was performed 24 h, 48 h and 72 h upon MYCN activation, including four biological replicates per condition.
2021-06-03 | E-MTAB-9667 | biostudies-arrayexpress
Project description:15,000 GFP+ cells were collected from two replicates of the Htr3a GFP line into RNAlater (ThermoFisher, AM7024). RNA was purified and bulk RNA-seq was performed using the Ovation RNA-seq system V2 (Nugen, 7102-32) Bulk RNA-seq analysis of Type 5 retinal bipolar cells (2 biological replicates)
2016-08-25 | E-GEOD-81902 | biostudies-arrayexpress
Project description:Targeted analysis of retinal-cysteine adduct in Opsin 5 like-1 (Opn5L1) protein
Chicken Opn5L1 E177K/Q192K mutant was expressed in HEK293T, regenerated by all-trans-retinal, solubilized by dodecyl maltoside, and purified using Rho1D4 antibody-conjugated Sephalose. Semi-quantitative targeted analyses of trypsinized Opn5L1 with or without light irradiation were carried out using reverse phase LC-ESI-MSn to detect light-dependent formation of retinal-cysteine adduct. The results were analyzed by Mass++, mMass and Igor Pro softwares.
2018-02-15 | PXD008890 | JPOST Repository
Project description:Single cell RNA-seq upon MYCN activation in the hTERT-immortalized MYCN retinal pigmented epithelial cell line (RPE1–MYCN-ER). The cell line was treated with tamoxifen (400nM; 4-OHT) for MYCN induction (with 4-OHT or not). Analysis was performed 22h, 23h, and 24 h upon MYCN activation.
2021-12-01 | E-MTAB-9689 | biostudies-arrayexpress
Project description:The ALK^F1174L mutation is associated with intrinsic and acquired resistance to crizotinib and cosegregates with MYCN in neuroblastoma. In this study, we generated a mouse model overexpressing ALK^F1174L in the neural crest. Comapred to mice expressing ALK^F1174L or MYCN alone, combined expression of the two aberrations led to development of neuroblastoma with a shorter latency and higher penetrance. Here, we evaluated the transcriptional profiles of MYCN-driven neuroblastomas with or without the expression of ALK^F1174L to determine the pathogenic consequences of the ALK^F1174L/MYCN interaction in neuroblastoma. 10 mice were analysed in this study. Five ALK^F1174L/MYCN tumors were compared with five MYCN tumors. Total RNA was extracted, samples were labeled and processed using the Agilent Low Input Quick Amp two color Cy3(sample) and Cy5 (mouse reference) labeling kit and hybridized to Agilent SurePrint G3 Mouse Gene Expression arrays.
2012-07-04 | E-GEOD-35560 | biostudies-arrayexpress
Project description:The ALK^F1174L mutation is associated with intrinsic and acquired resistance to crizotinib and cosegregates with MYCN in neuroblastoma. In this study, we generated a mouse model overexpressing ALK^F1174L in the neural crest. Comapred to mice expressing ALK^F1174L or MYCN alone, combined expression of the two aberrations led to development of neuroblastoma with a shorter latency and higher penetrance. Here, we evaluated the transcriptional profiles of MYCN-driven neuroblastomas with or without the expression of ALK^F1174L to determine the pathogenic consequences of the ALK^F1174L/MYCN interaction in neuroblastoma.
2012-07-05 | GSE35560 | GEO
Project description:Bulk RNA-sequencing of individual chicken otocysts, in which Notch activity was either stimulated or blocked. To stimulate Notch activity, the E2 otic placodes were in ovo transfected with a construct overexpressing Notch1 Intracellular domain (NICD1) or a control plasmid expressing mRFP1 and collected 6h or 24h later. To pharmacologically block Notch activity, E2.5 chicken otocysts were incubated in media enriched with γ-secretase Inhibitor or control condition (DMSO) for 6h or 24h. Transcripts abundance was mapped to a chicken reference genome using Kallisto package.
2022-12-01 | GSE196999 | GEO
Project description:Two genes have a synthetic lethal relationship when silencing or inhibition of one gene is only lethal in the context of a mutation or activation of the second gene. This situation offers an attractive therapeutic strategy, as inhibition of such a gene will only trigger cell death in tumor cells with an activated second oncogene but spare normal cells without activation of the second oncogene. Here we present evidence that CDK2 is synthetic lethal to neuroblastoma cells with MYCN amplification and overexpression. Neuroblastomas are childhood tumors with an often lethal outcome. Twenty percent of the tumors have MYCN amplification and these tumors are ultimately refractory to any therapy. Targeted silencing of CDK2 by three RNA interference techniques induced apoptosis in MYCN-amplified neuroblastoma cell lines, but not in MYCN single copy cells. Silencing of MYCN abrogated this apoptotic response in MYCN-amplified cells. Inversely, silencing of CDK2 in MYCN single copy cells did not trigger apoptosis, unless a MYCN transgene was activated. The MYCN induced apoptosis after CDK2 silencing was accompanied by nuclear stabilization of P53 and mRNA profiling showed up-regulation of P53 target genes. Silencing of P53 rescued the cells from MYCN-driven apoptosis. The synthetic lethality of CDK2 silencing in MYCN activated neuroblastoma cells can also be triggered by inhibition of CDK2 with a small molecule drug. Treatment of neuroblastoma cells with Roscovitine, a CDK inhibitor, at clinically achievable concentrations induced MYCN-dependent apoptosis. The synthetic lethal relation between CDK2 and MYCN indicates CDK2 inhibitors as potential MYCN-selective cancer therapeutics. CDK2 shRNA in a tet repressor system was stably transfected in the IMR32 cell line. Time course analysis was performed in triplicate after induction of CDK2 shRNA at 5 time points.
2014-05-19 | E-GEOD-16480 | biostudies-arrayexpress