Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Evaluation of mRNA expression changes upon TRAF4 mis-expression in HT1376 and T24 bladder cancer cell lines

ABSTRACT: TRAF4 is highly expressed in the epithelial bladder cancer cell line, HT1376 and poorly expressed in the mesenchymal cell line, T24. We evaluated the genetic changes in HT1376 upon TRAF4 knockdown using two independent shRNAs targetting TRAF4. The changes were documented with respect to the control cell line transduced with empty vector shRNA plasmid. Also, we over-expressed (myc-tagged) TRAF4 in T24 and evaluated mRNA changes with respect to cell line over-expressing empty vector with a myc-tag.

ORGANISM(S): Homo sapiens

PROVIDER: GSE161509 | GEO | 2020/11/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TRAF4 promotes the malignancy of ovarian high-grade serous carcinoma by activating YAP pathway

Project description:Ovarian high-grade serous carcinoma (HGSC) accounts for the majority of deaths caused by epithelial ovarian cancer. The precise molecular changes attributable for the pathogenesis of HGSC are still largely unknown. TRAF4 has been identified to be up-regulated in some cancers. However, the association between TRAF4 and the malignancy of HGSC has not been elucidated before. In this study, we aim to explore the prognostic value and function of TRAF4 in HGSC. The results of immunohistochemistry in 174 cases of HGSC showed that high expression of TRAF4 was significantly associated with a shorter overall survival (p=0.005) and recurrence-free survival (p=0.003) in HGSC. Knock-down of TRAF4 inhibited the malignancy of ovarian cancer cells, and over-expression of TRAF4 increased cell malignancy both in vitro and in vivo. Moreover, mechanism studies demonstrated that TRAF4 promoted cell malignancy by activating YAP pathway in HGSC. In conclusion, TRAF4 could be a prognostic biomarker for HGSC and increase HGSC cell malignancy by activating YAP pathway, which may serve as a potential therapeutic target for HGSC.

2022-05-15 | GSE202840 | GEO

Feedforward regulation of Myc coordinates lineage-specific with housekeeping gene expression during progenitor cell differentiation

Project description:Chromatin-associated RNA-Seq of pre-B cell line B3 transduced with Ikaros (Ikaros-ERt2) or Myc (Myc-ERt2) or Ikaros+Myc or control vector (Empty).

2019-03-01 | GSE125493 | GEO

Evaluation of mRNA expression changes upon TRAF4 mis-expression in HT1376 and T24 bladder cancer cell lines

Project description:Evaluation of mRNA expression changes upon TRAF4 mis-expression in HT1376 and T24 bladder cancer cell lines

| PRJNA678557 | ENA

Human BMSCs protein analysis that interact with TRAF4 during adipogenic differentiation

Project description:To explore the mechanism underlying the negative regulation of adipogenesis by TRAF4, we performed the LC-MS/MS experiments to identify the proteins that interact with TRAF4 during adipogenic differentiation.

2020-05-27 | PXD017524 | Pride

Total RNA-Seq in control and TRAF4-overexpressing LNCaP cells

Project description:We reported the total gene expression in control and TRAF4-overexpressing LNCaP cells

2023-02-17 | GSE225509 | GEO

Expression data for T24 bladder cancer cell line - scrambled, SOX4-KD and SOX4 overexpression

Project description:We knocked down SOX4 in T24 cell and created 3 cell lines: T24-scrambled, T24-SOX4-knockdown and T24-SOX4-rescue and compared gene expression changes SOX4 is a developmental transcription factor that is overexpressed in as many as 23% of bladder cancer patients, but the role of SOX4 in bladder cancer tumorigenesis is not well understood. Given SOX4’s many roles in embryonic development and context-dependent regulation of gene expression, we sought to understand SOX4’s contribution to bladder cancer and to elucidate SOX4 regulated genes that might contribute to tumorigenesis. We employed a CRISPR interference (CRISPRi) method to transcriptionally repress SOX4 expression in T24 bladder cancer cell lines, rescued these cell lines with lentivirally expressed SOX4, and performed whole genome expression profiling. SOX4 knockdown cells exhibited decreased invasive capabilities but no changes in migration or proliferation, while rescue with SOX4 lentiviral vector restored the invasive phenotype. Gene expression profiling revealed 173 high confidence SOX4 regulated genes

2018-08-16 | GSE118572 | GEO

Genome-wide AR binding under androgen deprivation condition upon TRAF4 overexpression

Project description:We report that TRAF4-mediated AR ubiquitination alters AR genomic binding profile under androgen deprivation condition.

2023-05-24 | GSE154001 | GEO

Difference of DNA methylation and Chromatin accessibility of T24 SP cell and T24 NSP cell

Project description:Difference of DNA methylation and Chromatin accessibility of T24 SP cell and T24 NSP cell

2020-01-30 | GSE130641 | GEO

Gene expression profileing of DDR1 overexpression and control T24 human bladder cancer cell line

Project description:We performed RNA-seq analysis on xenograft mouse model generated by T24 human bladder cancer cell line with enforced expression of DDR1 or controls.

2022-10-19 | GSE191097 | GEO

Total RNA-Seq in TRAF4-overexpressing castration-resistant xenograft tumors and the control castration-responsive tumors

Project description:We reported the tumor total gene expression TRAF4-overexpressing castration-resistant xenograft tumors and the control castration-responsive tumors

2020-07-15 | GSE154029 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data