Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Implications of TEAD4 in Metabolic Processes of Gastric Cancer [Bisulfite-Seq]

ABSTRACT: Gastric cancer (GC) is a prevalent malignancy worldwide, imposing a significant global health burden. Despite the development of various treatment strategies, effective management of GC remains elusive. Consequently, extensive research efforts have been directed towards uncovering the underlying molecular mechanisms of GC pathogenesis to develop novel and targeted therapeutic approaches. Among the identified signaling pathways, the Hippo pathway has emerged as a critical contributor to tumor development and acquired drug resistance in GC. It also interacts with multiple other pathways implicated in GC progression. Recent studies have highlighted the role of abnormal DNA methylation patterns in the early stages of GC development, rather than being confined to advanced stages. Specifically, the Hippo pathway member TEAD4 which is implicated in all four GC molecular subtypes, as classified by The Cancer Genome Atlas (TCGA) project, has been found to be hypomethylated in GC. In our research, we employed targeted hypermethylation using a combination of KRAB and DNMT3AL EpiEffectors to achieve epigenetic silencing of the TEAD4 promoter. Post-intervention, consistent with previous studies, we observed a reduction in the cancerous properties of the manipulated GC cells, such as proliferation, colony formation ability, migration, and invasion. Interestingly, transcriptomics results suggest that TEAD4 suppression may imply the downregulation of several carbohydrate-related metabolic pathways, DNA replication and repair mechanisms, as well as carbon metabolism. These findings may offer deeper insights into the multifaceted roles of TEAD4 in the progression of GC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE299322 | GEO | 2026/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Implications of TEAD4 in Metabolic Processes of Gastric Cancer [RNA-Seq]

Project description:Gastric cancer (GC) is a prevalent malignancy worldwide, imposing a significant global health burden. Despite the development of various treatment strategies, effective management of GC remains elusive. Consequently, extensive research efforts have been directed towards uncovering the underlying molecular mechanisms of GC pathogenesis to develop novel and targeted therapeutic approaches. Among the identified signaling pathways, the Hippo pathway has emerged as a critical contributor to tumor development and acquired drug resistance in GC. It also interacts with multiple other pathways implicated in GC progression. Recent studies have highlighted the role of abnormal DNA methylation patterns in the early stages of GC development, rather than being confined to advanced stages. Specifically, the Hippo pathway member TEAD4 which is implicated in all four GC molecular subtypes, as classified by The Cancer Genome Atlas (TCGA) project, has been found to be hypomethylated in GC. In our research, we employed targeted hypermethylation using a combination of KRAB and DNMT3AL EpiEffectors to achieve epigenetic silencing of the TEAD4 promoter. Post-intervention, consistent with previous studies, we observed a reduction in the cancerous properties of the manipulated GC cells, such as proliferation, colony formation ability, migration, and invasion. Interestingly, transcriptomics results suggest that TEAD4 suppression may imply the downregulation of several carbohydrate-related metabolic pathways, DNA replication and repair mechanisms, as well as carbon metabolism. These findings may offer deeper insights into the multifaceted roles of TEAD4 in the progression of GC.

2026-07-31 | GSE299321 | GEO

A splicing switch of TEAD4 regulates Hippo-YAP signaling pathway to inhibit tumor proliferation

Project description:Splicing dysregulations extensively occur in cancers, yet the biological consequences of such alterations are mostly undefined. Here we report that the Hippo-YAP signaling, a key pathway that regulates cell proliferation and organ size, is under control of a new splicing switch. We show that TEAD4, the transcription factor that mediates Hippo-YAP signaling, undergoes alternative splicing facilitated by the tumor suppressor RBM4, producing a truncated isoform, TEAD4-S, which lacks N-terminal DNA-binding domain but maintains YAP-interaction domain. TEAD4-S is located in both nucleus and cytoplasm, acting as a dominant negative isoform to YAP activity. Consistently, TEAD4-S is reduced in cancer cells, and its re-expression suppresses cancer cell proliferation and migration, inhibiting tumor growth in xenograft mouse model. Furthermore, TEAD4-S is reduced in human cancers, and patients with elevated TEAD4-S levels have improved survival. Altogether these data reveal a novel RBM4-mediated splicing switch that serves to fine-tune Hippo-YAP pathway. Cell lines stably expressing YAP, YAP/TEAD4-S, YAP/TEAD4-FL, YAP/RBM4 and control vector were created, and the total RNA was purified from the cells using TRIzol reagents. The polyadenylated RNAs were purified for construction of sequencing library using kapa TruSeq Total RNA Sample Prep kits (UNC High Throughput Sequencing Facility).

2016-06-16 | E-GEOD-80372 | biostudies-arrayexpress

TEAD4

Project description:TEAD4

| PRJNA604980 | ENA

The Role and Mechanism of TEAD4 in Preimplantation Embryonic Development in Mice and Cattle

Project description:Tead4 is a critical transcription factor expressed during preimplantation development and is essential for the expression of trophectoderm-specific genes in mice. However, the mechanism of Tead4’s function in mouse preimplantation development and its conservation across mammals remains unclear. Here, we report that Tead4 is a crucial transcription factor necessary for blastocyst formation in mice. Disruption of TEAD4 through base editing results in developmental arrest at the morula stage. Additionally, RNA-seq analysis reveals dysregulation of 670 genes in Tead4 knockout embryos. As anticipated, Tead4 knockout leads to a decrease in trophectoderm genes CDX2 and GATA3. Intriguingly, we observed a reduction in KRT8, suggesting that Tead4 influences the integrity of the trophectoderm epithelium in mice. More importantly, we noted a decrease in nuclear YAP for Tead4-deficient embryos, indicating that Tead4 directly regulates Hippo signaling. In contrast, bovine embryos with TEAD4 depletion can still develop to blastocysts with normal expression of CDX2, GATA3, and SOX2, albeit with a decrease in total cell number and ICM cell number. In conclusion, we propose that Tead4 regulates mouse blastocyst formation via Krt8 and Yap, both of which are critical regulators of mouse preimplantation development.

2024-07-15 | GSE237418 | GEO

A splicing switch of TEAD4 regulates Hippo-YAP signaling pathway to inhibit tumor proliferation

2016-06-16 | GSE80372 | GEO

AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [expression]

Project description:Embryonic blood cell development occurs via well-defined developmental stages which are recapitulated in vitro by differentiation of embryonic stem cells. This process is tightly regulated by the interaction of tissue- specific and ubiquitous transcription factors with the chromatin landscape in response to outside signals. We previously identified binding motifs for the commonly expressed AP-1 transcription factor family in open chromatin regions specific for early stages of blood specification and thus aimed to study the role of AP-1 for hemangioblast differentiation. Here we show that FOS and JUN together bind to and activate a core set of vascular genes in the hemogenic endothelium and that upon global inhibition of AP-1 by expression of a dominant negative FOS peptide the balance between endothelial and hematopoietic fate is shifted towards blood. Moreover, we demonstrate that in the hemogenic endothelium AP-1 is required for de novo binding of TEAD4, a transcription factor connected to Hippo signaling, to vascular genes. Notably, after the endothelial-to-hematopoietic transition TEAD4 binding is no longer persisting. These findings provide novel mechanistic insights into vascular and hematopoietic development.

2016-10-21 | GSE79322 | GEO

AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [DNase-Seq]

2016-10-21 | GSE79321 | GEO

AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [ChIP-Seq]

2016-10-21 | GSE79320 | GEO

TEAD4 occupied genes in differentiated C2C12 myoblasts

Project description:The TEAD (1-4) transcription factors comprise the conserved TEA/ATTS DNA binding domain recognising the MCAT element in the promoters of muscle-specific genes. Despite extensive genetic analysis, the function of TEAD factors in muscle differentiation has proved elusive due to redundancy amongst the family members. Expression of the TEA/ATTS DNA binding domain that acts a dominant negative repressor of TEAD factors in C2C12 myoblasts inhibits their differentiation, while selective shRNA knockdown of TEAD4 results in abnormal differentiation characterised by the formation of shortened myotubes. Chromatin immunoprecipitation coupled to array hybridisation (ChIP-chip) shows that TEAD4 occupies 867 promoters including those of myogenic miRNAs. We show that TEAD factors cooperate with MYOD1 to directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation and fusion. RNA-seq identifies a novel set of TEAD4 target genes encoding muscle structural and regulatory proteins and those required for the unfolded protein response. In contrast, TEAD4 represses expression of the growth factor CTGF and Cyclin D1 to promote differentiation. Together these results show that TEAD factor activity is essential for C2C12 cell differentiation and define a novel and nonredundant role for TEAD4 in regulating the unfolded protein response. C2C12 cells were infected with retrotiviral vector expressing Flag-HA-Tagged TEAD4 or with empty control vector and selected in the continouos presence of puromycin. Infected cell populations were then differentiated for 5 days in DMEM medium with 2% horse serum and fixed in 0.4% formaldehyde.

2011-08-21 | E-GEOD-29208 | biostudies-arrayexpress

Identification of TEAD4 target genes in colorectal cancer cells

Project description:We have identified TEAD4 as a key prognosis factor in colorectal cancer. To elucidate the potentail mechanism and function of TEAD4 in colorectal caner, we generated two stable cell lines expressing different shRNA targeting TEAD4 in the mesenchymal-like LoVo cells and the differential genes were detected by microarray. LoVo colorectal cancer cells stably expressing pLKO.1 control shRNA or sh1_shTEAD4 or sh2_shTEAD4

2014-01-01 | E-GEOD-53063 | biostudies-arrayexpress

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