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RNA-seq of PTEN knockdown in GL261 cells

ABSTRACT: RNA-seq of PTEN knockdown in GL261 cells

PROVIDER: PRJNA661466 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12588820_1.fastq.gz	Fastqsanger.gz
	SRR12588820_2.fastq.gz	Fastqsanger.gz
	SRR12588821_1.fastq.gz	Fastqsanger.gz
	SRR12588821_2.fastq.gz	Fastqsanger.gz
	SRR12588822_1.fastq.gz	Fastqsanger.gz

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RNA-seq of PTEN knockdown in GL261 cells

Project description:PTEN deficiency is known to lead to tumor-intrinsic resistance to immune checkpoint blockade (ICB) treatment, especially in glioblastoma (GBM). We used RNA sequence to study the global gene expression and identified differentially expressed genes in PTEN knockdown GL261 cells, aiming to identify genes and pathways that are regulated by PTEN.

2021-03-06 | GSE157488 | GEO

Effect of depletion of PTEN on gene expression of GL261 cells

Project description:To predict the COCA subtype by gene expression, we established GL261 cell lines in which PTEN has been knocked out by sgRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells.

2022-09-30 | GSE214398 | GEO

Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

Project description:GL261 cells are one of the most common mouse glioblastoma cells used for in vivo studies in a immunocompetent model. We analyze GL261 and stem cells derived from them (GL261-GSCs) using scRNA-Seq.

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Effect of depletion of PTEN on gene expression of GL261 cells

Project description:Effect of depletion of PTEN on gene expression of GL261 cells

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Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

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Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

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Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

Project description:GL261 cells are one of the most common mouse glioblastoma cells used for in vivo studies in a immunocompetent model.

2024-03-28 | GSE246262 | GEO

Knockdown of CUL3 and PTEN in A549 lung adenocarcinoma cells

Project description:Non-small cell lung cancers (NSCLCs) harbor thousands of passenger events that hide genetic drivers. Even highly recurrent events in NSCLC, such as mutations in PTEN, EGFR, KRAS, and ALK, are only detected in, at most, 30% of patients. Thus, many unidentified low-penetrant events are causing a significant portion of lung cancers. To detect low-penetrance drivers of NSCLC a forward genetic screen was performed in mice using the Sleeping Beauty (SB) DNA transposon as a random mutagen to generate lung tumors in a Pten deficient background. SB mutations coupled with Pten deficiency were sufficient to produce lung tumors in 29% of mice. Pten deficiency alone, without SB mutations, resulted in lung tumors in 11% of mice, while the rate in control mice was ~3%. In addition, thyroid cancer and other carcinomas as well as the presence of bronchiolar and alveolar epithelialization in mice deficient for Pten were also identified. Analysis of common transposon insertion sites identified 76 candidate cancer driver genes. These genes are frequently dysregulated in human lung cancers and implicate several signaling pathways. Cullin3 (Cul3), a member of an ubiquitin ligase complex that plays a role in the oxidative stress response pathway, was identified in the screen and evidence demonstrates that Cul3 functions as a tumor suppressor HumanHT-12 v4 Expression BeadChip Kit for human A549 lung adenocarcinoma cells with CUL3, PTEN, CUL3 and PTEN or no knockdown. A549 cells were stably transfected under Puromycin or Hygromycin selection to knockdown PTEN (SA Biosystems) or CUL3 (Open Biosystems) shRNAs. RNA was extracted in triplicate from each condition and used for microarray

2015-05-15 | E-GEOD-68869 | biostudies-arrayexpress

BRG1 occupancy profiling by high throughput sequencing from control and PTEN knockdown 22RV-1 cells

Project description:To identify the downstream targets and pathways mediated by BRG1, chromatin immunoprecipitation followed by sequencing (ChIP–seq) was performed in control and PTEN-knockdown 22RV-1 cells. Total 6279 genes showed the enhanced BRG1 occupancies in PTEN-knockdown cells as compared to that in control cells. Genome-wide analysis revealed that PTEN loss lead to increase BRG1 intervals specifically localized at enhancers, but not distal promoter regions. We therefore reasoned ablation of BRG1 might impair enhancer configurations in PTEN-deficient cells.

2019-01-14 | GSE115615 | GEO

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Project description:Intrahepatic cholangiocarcinoma (ICC) is known to have a poor prognosis among primary liver cancers. We created a vitro model of cholangiocarcinogenesis using HepG2 with specifically knockdown of Pten and Traf3. RNA sequence was performed with RNA extracted from the liver of mice lacking liver-specific Pten and Traf3.

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