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Links from GEO DataSets

Items: 20

1.

Liaison between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion-Negative Rhabdomyosarcoma

(Submitter supplied) Rhabdomyosarcoma (RMS) is a pediatric malignancy of mesenchymal origin. Fusion Negative-RMS (FN-RMS) tumors are associated with RAS-pathway activation. RMS tumors express pro-differentiation myogenic transcription factors MYOD and MYOG, yet why they are unable to differentiate is poorly understood. Here we show that SNAI2 is highly expressed in FN-RMS, is regulated by MYOD and blocks myogenic differentiation promoting growth. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other
Platform:
GPL18573
22 Samples
Download data: HIC, NARROWPEAK, TXT
2.

RNA-Seq and ChIP-Seq in SIX1 deficient Rhabdomyosarcoma cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL24676
21 Samples
Download data: TDF
Series
Accession:
GSE173155
ID:
200173155
3.

Chromatin states and transcription factor binding in SIX1 deficient Rhabdomyosarcoma cells

(Submitter supplied) Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed SIX1, MYOD1, and H3K27ac ChIPseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptional activity and myogenic transcription factor binding in fusion-negative Rhabdomyosarcoma.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: TDF
Series
Accession:
GSE173151
ID:
200173151
4.

Transcriptomes of SIX1 deficient and control Rhabdomyosarcoma cells

(Submitter supplied) Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: TXT
5.

Epigenetic Reprogramming of mutant RAS-driven Rhabdomyosarcoma via MEK Inhibition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL1261 GPL18573 GPL11154
60 Samples
Download data: BED, CEL, FPKM_TRACKING
Series
Accession:
GSE85171
ID:
200085171
6.

MEK inhibition rewires enhancer landscapes in RAS-driven Rhabdomyosarcoma to unlock a myogenic differentation block

(Submitter supplied) Trametinib-treated rhabdomyosarcoma cells undergo transcriptional reprogramming akin to myogenic differentiation. This reprogramming is induced by loss of ERK-mediated inhibition of MYOG expression. Restoration of MYOG allows establishment of super-enhancers at genes expressed by terminally differentiated myotubes. Our findings demonstrate that aberrant MAP kinase activity blocks differentiation in rhabdomyosarcoma and highlight trametinib as a potential therapeutic for RAS-mutated rhabdomyosarcoma.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: FPKM_TRACKING
7.

MEK inhibition profoundly reprograms myogenic super enhancers in mutant-RAS driven Rhabdomyosarcoma

(Submitter supplied) Trametinib-treated rhabdomyosarcoma cells undergo transcriptional reprogramming akin to myogenic differentiation. This reprogramming is induced by loss of ERK-mediated inhibition of MYOG expression. Restoration of MYOG allows establishment of super-enhancers at genes expressed by terminally differentiated myotubes. Our findings demonstrate that aberrant MAP kinase activity blocks differentiation in rhabdomyosarcoma and highlight trametinib as a potential therapeutic for RAS-mutated rhabdomyosarcoma.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
38 Samples
Download data: BED
Series
Accession:
GSE85169
ID:
200085169
8.

Oncogenic RAS blocks myogenic differentiation

(Submitter supplied) C2C12 mouse myoblasts expressing RAS mutants identified in human tumors fail to differentiate in low serum media.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
4 Samples
Download data: CEL
Series
Accession:
GSE85168
ID:
200085168
9.

CASZ1 directly regulates expression of myogenic genes through regional epigenetic modifications to induce muscle and rhabdomyosarcoma cell differentiation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
6 related Platforms
57 Samples
Download data: BW
Series
Accession:
GSE126147
ID:
200126147
10.

RNA-sequencing analysis to investigate genes regulated by CASZ1 in RD cells

(Submitter supplied) In this study we identified genes regulated by CASZ1b in RD cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TXT
11.

RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

(Submitter supplied) In this study we identified genes regulated by CASZ1b in SMS-CTR cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
10 Samples
Download data: TXT
12.

RNA-sequencing analysis to investigate genes regulated by CASZ1 in C2C12 cells

(Submitter supplied) In this study we identified genes regulated by CASZ1b in C2C12 cells
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL21493 GPL21103
15 Samples
Download data: TXT
Series
Accession:
GSE126144
ID:
200126144
13.

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

(Submitter supplied) MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
4 Samples
Download data: BW
Series
Accession:
GSE126143
ID:
200126143
14.

Genome-wide mapping of CASZ1b binding sites and investigate its effect on chromatin status in SMS-CTR cells [CTRtetCASZ1b]

(Submitter supplied) In SMS-CTR cells, we identified genomewide binding sites of CASZ1b. The overexpression of CASZ1b in SMS-CTR cells led to a regional epigenetic modification.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
14 Samples
Download data: BW
Series
Accession:
GSE126142
ID:
200126142
15.

The affect of loss of Casz1 in C2C12 cells on super-enhancers

(Submitter supplied) In the differereniated C2C12 cells, knockdown of Casz1 leads to a re-establishment of super-enhancers
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: BW
Series
Accession:
GSE126141
ID:
200126141
16.

Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

(Submitter supplied) In SMS-CTR cells, the overexpression of CASZ1b in SMS-CTR cells led to a modification of regional chromation accessibility.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: BW
Series
Accession:
GSE126140
ID:
200126140
17.

Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

(Submitter supplied) Integrated analysis of genome-wide ChIP-Seq and RNA-Seq data revealed the first dynamic chromatin and transcriptional landscape of Twist2 binding during myogenic differentiation. During differentiation, Twist2 competes with MyoD at shared DNA motifs to direct global gene transcription and repression of the myogenic program. Additionally, TWIST2 shapes the epigenetic landscape to drive chromatin opening at oncogenic loci and chromatin closing at myogenic loci. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
34 Samples
Download data: BIGWIG
Series
Accession:
GSE127998
ID:
200127998
18.

P/CAF mediates Pax3-FKHR dependent oncogenesis in alveolar rhabdomyosarcoma

(Submitter supplied) Analysing the differential expression of various genes upon knockdown of acetyltransferase P/CAF in Rh31 to identify its targets
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
6 Samples
Download data: TXT
Series
Accession:
GSE69443
ID:
200069443
19.

A MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2 targeting [Hi-ChIP]

(Submitter supplied) Rhabdomyosarcoma (RMS) is a pediatric mesenchymal-derived malignancy encompassing Fusion Positive (FP)-RMS expressing PAX3/7-FOXO1 and Fusion Negative (FN)-RMS often mutated in the RAS pathway. RMS expresses the master myogenic transcription factor MYOD that, paradoxically, is unable to support differentiation while essential for tumor cell survival. We identify here SKP2, an oncogenic E3-ubiquitin ligase, as a critical driver of tumorigenesis in FN-RMS. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL24676
2 Samples
Download data: HIC
Series
Accession:
GSE245495
ID:
200245495
20.

A MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2 targeting

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
10 Samples
Download data: BED, HIC, TXT
Series
Accession:
GSE241283
ID:
200241283
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