Mouse neuroblastoma Tcof1
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE1956 | GEO | 2004/11/11
SECONDARY ACCESSION(S): PRJNA90903
REPOSITORIES: GEO
Similar Datasets
Project description:Genomewide analysis of gene expression associated with Tcof1 in mouse neuroblastoma. NB N1E-115 cells with wildtype, overexpression, knockdown of Tcof1.
2007-11-06 | E-GEOD-1956 | biostudies-arrayexpress
Project description:ALK is a tyrosine kinase receptor and oncogene in neuroblastoma (NB). The receptor is activated by the ALKAL2 ligand, but it is unknown whether missregulation of this ligand may play a role in NB carcinogenesis. Here, a TH-MYCN driven neuroblastoma mice was created +/- ALK F1178S mutation and +/- ALKAL2 overexpression
2020-11-24 | E-MTAB-9600 | biostudies-arrayexpress
Project description:BMI1 is a polycomb protein and its overexpression has been correlated with cancer development and aggressiveness. We previously reported that v-myc avian myelocytomatosis viral oncogene neuroblastoma-derived homolog (MYCN)-induced BMI1 positively regulated neuroblastoma (NB) cell proliferation via the transcriptional suppression of tumor suppressors in NB cells. In order to evaluate the potential of BMI1 as a new target for NB therapy, we herein examined the effects of BMI1 reductions on NB cell differentiation and apoptotic NB cell death. BMI1 knockdown (KD) up to 7 days in NB cells significantly induced their differentiation. BMI1 depletion up to 14 days significantly induced apoptotic NB cell death along with the activation of p53, increases in p73, and induction of p53 family downstream molecules. BMI1 depletion in vivo markedly suppressed NB xenograft tumor growth. A pathological analysis using the TUNEL assay indicated the induction of apoptotic cell death. BMI1 reductions activated ATM and increased γ-H2AX in NB cells. Importantly, these DNA damage signals and apoptotic cell death were not canceled by transduction of polycomb group molecules EZH2 and RING1B. Further, EZH2 or RING1B knockdown could not induce apoptotic NB cell death at the same level of BMI1 KD. Together, BMI1 appears to be a promising target of molecular therapy for NB tumors and our report clarified, for the first time, the shared role of PcG proteins in DNA damage response of NB cells.
2022-11-08 | GSE189449 | GEO
Project description:<p>Neuroblastoma is the most common extra-cranial solid tumor in children. It represents 8% to 10% of all childhood cancers. Stage 4 Neuroblastoma is characterized by its clinical heterogeneous outcome. The special category, stage 4S tumors (2-5% of all NB) are chemo-sensitive, and the patients show spontaneous regression. On the other hand, MYCN amplification (25-30% of all NB) is associated with poor outcome of neuroblastoma, thus we further categorize stage 4 neuroblastoma into MYCN non-amplified and MYCN amplified group. Here we use transcriptome sequencing to characterize the transcriptome in 29 stage 4 Neuroblastoma samples.</p>
| phs000868 | dbGaP
Project description:Recent research has underscored the significance of circular RNA (circRNA) in various cancers, including neuroblastoma (NB). Specifically, circ-SHPRH, a distinct circRNA, has emerged as an inhibitor of tumor growth through its ability to sequester miRNAs or produce the SHPRH-146aa protein. To explore circ-SHPRH's involvement in NB and its potential application in gene therapy, this study examined its expression in 94 NB tissues and cell lines (SK-N-BE(2), SH-SY5Y, CHLA-255) using real-time PCR and fluorescence in situ hybridization (FISH). Functional assays encompassing both overexpression and knockdown experiments in NB cell lines, as well as in vivo investigations, were conducted. RNA-seq analysis revealed a correlation between circ-SHPRH and the P21 (CDKN1A) pathway, a pivotal cell cycle regulator. Validation through PCR and other techniques confirmed that circ-SHPRH upregulated P21 expression. Furthermore, the regulatory role of circ-SHPRH in the P21-CDK pathway was corroborated through SHPRH-146aa expression. Notably, adenovirus-mediated overexpression of circ-SHPRH effectively curbed NB tumor growth in NSG mice, while combining circ-SHPRH with everolimus exhibited potential for NB treatment. This study elucidates the remarkable significance of circ-SHPRH in NB and its prospective utility in gene therapy, thereby paving the way for innovative therapeutic approaches.
2024-07-19 | GSE244294 | GEO
Project description:ALK is a tyrosine kinase receptor and oncogene in neuroblastoma (NB). The receptor is activated by the ALKAL2 ligand, but it is unknown whether missregulation of this ligand may play a role in NB carcinogenesis. To characterize the transcriptomic response to ALKAL2 in neuroblastoma cell lines, RNA-Seq was performed on NB1 and IMR32 human NB cell lines.
2020-11-24 | E-MTAB-9598 | biostudies-arrayexpress
Project description:In the present study we investigated the structure of MYCN amplifications, examples of both dmin and hsr, in eight neuroblastoma (NB) and two small cell lung carcinoma (SCLC) cell lines. Ten cell lines were analyzed for gene amplification: STA-NB3 (NB), STA-NB4 (NB), STA-NB8 (NB), STA-NB10DM (NB), STA-NB10HSR (NB), STA-NB13 (NB), STA-NB15 (NB), SK-N-BE (NB), GLC8 (SCLC), GLC14 (SCLC). NimbleGen human reference sample was used as reference DNA.
2010-06-10 | E-GEOD-22279 | biostudies-arrayexpress
Project description:We report a previously unrecognized role of SAPCD2 in E2F signaling pathway in neuroblastoma. To explore SAPCD2-dependent gene regulation, RNA-seq analysis was conducted and the differently expressed genes were revealed in the SAPCD2-knockdown SK-N-BE(2) cells in comparison to control group. We find that SAPCD2 contributes to E2F7 mislocalization and decreases the level of nuclear E2F7 in NB cells, thus restraining the inhibitory effect of nuclear E2F7 on E2F signaling pathway. SAPCD2 knockdown limits the overactivation of E2F signaling in NB cells, affects the expression of genes involved in cell cycle and chromosome stability, and thereby blocking tumor progression.
2022-01-23 | GSE186245 | GEO
Project description:Circular RNAs (circRNAs), a noncoding RNA class originating from alternative splicing, are highly abundant in neural tissues and were shown to regulate gene expression e.g. by interacting with microRNAs and RNA-binding proteins. Neuroblastoma is an embryonal neoplasia, which arises from undifferentiated neural crest cells. Here, we aimed to explore, whether circRNAs influence the pathogenesis of high-risk neuroblastoma. We performed whole-transcriptome sequencing of 104 primary neuroblastoma samples of all risk-groups and identified 5,203 unique circRNAs involving 2,302 genes. Candidate circRNA expression did not correlate with host gene expression, indicating independent regulatory mechanisms. circRNAs were significantly downregulated in the MYCN-amplified high-risk tumors. These findings were independently reproduced in a tetracycline-inducible MYCN-overexpression system based on a non MYCN-amplified neuroblastoma cell line, suggesting that MYCN drives this global circRNA repression. We identified the RNA helicase DHX9 as a mediator of this global suppressive effect of MYCN on circRNAs. Comparing our RNA sequencing data with other cancers and controls revealed a circRNA subset specifically upregulated in neuroblastoma that included a circRNA derived from the ARID1A tumor suppressor gene. Specific circARID1A knockdown resulted in reduced proliferation, cell numbers and viability, prompted apoptosis and induced a differentiated phenotype. Neither knockdown, nor overexpression of circARID1A influenced ARID1A mRNA and protein levels significantly. To dissect the potential mode of function, we performed a pulldown assay with subsequent mass spectrometry. We identified the RNA-binding protein KHSRP as an interaction partner that participates in the mechanism of action of circARID1A. In summary, this study highlights an important role of circRNAs in neuroblastoma biology and may establish this RNA class as a future therapeutic target and biomarker.
2023-04-06 | PXD026053 | Pride