Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differential effects of estrogen receptor beta isoforms on glioblastoma progression

ABSTRACT: Differential effects of estrogen receptor beta isoforms on glioblastoma progression

PROVIDER: PRJNA412261 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6078680.fastq.gz	Fastqsanger.gz
	SRR6078682.fastq.gz	Fastqsanger.gz
	SRR6078674.fastq.gz	Fastqsanger.gz
	SRR6078684.fastq.gz	Fastqsanger.gz
	SRR6078675.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Differential effects of estrogen receptor beta isoforms on glioblastoma progression

Project description:We examined the transcriptional changes modulated by knocking out ERβ and reintroduction of ERβ1 and ERβ5 isoforms by perfroming global transcriptome analysis. ERβ was knocked out in U87 cells using CRISPR/Cas9 system and reintroduced the ERβ1 and ERβ5 isoforms in knockout background. RNA was isolated from control U87, U87-ERβ-KO, U87-ERβ1 and U87-ERβ5 cells and utilized for RNA-seq analysis. Our results demonstrated that ERβ-KO, ERβ1 and ERβ5 modulated unique pathways including NF-κB singaling, Jak/STAT pathway and mTOR signaling.

2018-04-10 | GSE104296 | GEO

Differential Effects of Estrogen Receptor β Isoforms on Glioblastoma Progression.

Project description:The estrogen receptor β (ERβ) functions as a tumor suppressor in glioblastoma (GBM) cells. However, the in vivo significance of endogenous ERβ and the roles of its isoforms in GBM are incompletely understood. Using ERβ isoform-specific PCR screening, we found that GBM cells predominantly express ERβ1 and ERβ5, along with low levels of ERβ2 and ERβ4. We observed greater ERβ5 expression in higher grades of glioma than in lower grades. In CRISPR-based ERβ knockout (KO) cells and ERβ KO cells uniquely expressing ERβ1 or ERβ5 only, ERβ1 significantly reduced proliferation. Compared with parental GBM cells, ERβ KO cells exhibited high migratory and invasive potentials, and reexpression of ERβ1 resulted in the reduction of this phenotype. Interestingly, ERβ5 expression increased foci formation and anchorage-independent growth of NIH3T3 cells and increased motile structure formation, including filopodia and ruffles in GBM cells. Only ERβ1-expressing tumors resulted in longer mouse survival. RNA-Seq analysis revealed unique pathways modulated by ERβ1 and ERβ5. Compared with ERβ KO cells, ERβ1 cells exhibited lower activation of mTOR signaling molecules, including p-mTOR, p-S6K, and p-S6, and ERβ5-expressing cells had enhanced mTOR downstream signaling. Unique proteins including several that function as regulators of mTOR, immunomodulatory, and apoptosis pathways bound to ERβ1 and ERβ5 isoforms. Our work confirms the tumor-suppressive potential of ERβ1 and reveals the acquired oncogenic ability of ERβ5 in GBM cells. ERβ isoform status and their unique interactions with oncogenic pathways may have important implications in GBM progression.Significance: These findings suggest that only ERβ isoform 1 has tumor suppressor function in GBM and that ERβ isoform switching contributes to GBM progression. Cancer Res; 78(12); 3176-89. ©2018 AACR.

| S-EPMC6004261 | biostudies-literature

Progesterone Receptor Isoforms, Agonists and Antagonists Differentially Reprogram Estrogen Signaling.

Project description:Progesterone Receptor Isoforms, Agonists and Antagonists Differentially Reprogram Estrogen Signaling.

| PRJNA319518 | ENA

Estrogen inhibits the progression of liver cancer by modulating PRDX-induced ferroptosis

Project description:Liver cancer exhibits significant gender disparities, with men having a 2-5 times higher risk of developing liver cancer compared to women. Numerous studies have demonstrated the influence of estrogen on liver cancer development, although the precise underlying mechanism remains unclear. Peroxiredoxins (PRDXs) represent a recently identified peroxidase family that modulates various signaling pathways associated with reactive oxygen species. This research aims to explore the impact of estrogen on the expression of PRDX1, PRDX5, and PRDX6 in hepatocellular carcinoma cells, thereby modulating liver cancer progression. Treatment with estrogen and the silencing of PRDX1, PRDX5, and PRDX6 impairs the proliferative capacity of hepatocarcinoma cells. The levels of PRDX1, PRDX5, and PRDX6 were found to be elevated in hepatocellular carcinoma compared to normal tissues, with estrogen demonstrating the ability to decrease their expression in hepatocellular carcinoma cells. Furthermore, estrogen influences the expression of PRDXs (PRDX5 and PRDX6) by regulating RASA1. Additionally, estrogen stimulation impacts ferroptosis in hepatocellular carcinoma cells, suggesting that PRDXs and ferroptosis-related genes are estrogen-responsive genes that promote liver cancer progression. Elevated LPCAT3 levels and downregulation of PRDX1, PRDX5, and PRDX6 expression may potentially manage the advancement of HCC.

2024-08-26 | PXD055317 |

Interactome of different isoforms of RPL22L1 protein in human glioblastoma cells

Project description:Interactome of different isoforms of RPL22L1 protein in human glioblastoma cells

| PRJNA748369 | ENA

Differential gene methylation in paired glioblastomas suggests a role of microenvironment in tumor progression

Project description:We sought to analyze DNA methylation levels in paired (initial and recurrence) primary glioblastoma samples to identify candidate pathways that may prone to glioblastoma progression. This study investigates the dynamics of methylation in paired primary GBM.

2015-08-10 | E-MTAB-3476 | biostudies-arrayexpress

Differential expressed miRNAs between tumor tissues and adjecent normal tissues from a patient with glioblastoma

Project description:Glioblastoma is the most aggressive and lethal malignant brain tumor. miRNA expression profiling could be useful in improving the classification of tumors and predicting their behavior. In this study, the miRNA expression patterns in glioblastoma tumor tissues and adjacent normal tissues were identified through expression profiling of a patient with glioblastoma. The results will hopefully enhance our understandings of the epigentic changes in glioblastoma progression and provide candidates for miRNAs-based targeting tharapy. A paired miRNAs tumor tissues and adjacent tissues of a glioblastoma patient was used in this study. miRNAs were isolated using miRNeasy FFPE Kit (Qiagen). Profiling was established by applying the Agilent human miRNA Microarray (8 M-CM-^W 60K, v16.0) (Agilent Technologies).

2014-09-17 | E-GEOD-61445 | biostudies-arrayexpress

EGFR and EGFRvIII coopt host defense pathways, promoting progression in glioblastoma

Project description:Co-amplification of EGFR and EGFRvIII, a tumor-specific truncation mutant of EGFR, represent hallmark genetic lesions in glioblastoma. We report that EGFR and EGFRvIII stimulate the innate immune defense receptor Toll-like Receptor 2 (TLR2); and that knockdown of TLR2 led to a dramatic survival advantage in glioblastoma xenografts. EGFR and EGFRvIII activated TLR2 in a ligand-independent manner, promoting tumor growth and immune evasion. We show that EGFR and EGFRvIII cooperate to activate the Rho-associated protein kinase ROCK2, modulating malignant progression both by activating TLR2 and WNT signaling, and through remodeling the tumor microenvironment.

2024-11-26 | PXD034586 | Pride

Piwil1 Regulates Glioma Stem Cell Maintenance and Glioblastoma Progression

Project description:Piwil1 Regulates Glioma Stem Cell Maintenance and Glioblastoma Progression

| PRJNA673195 | ENA

Reticulocalbin 3 is a Novel Mediator of Glioblastoma Progression

Project description:Reticulocalbin 3 is a Novel Mediator of Glioblastoma Progression

| PRJNA942618 | ENA