Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance

ABSTRACT: Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance

PROVIDER: PRJNA594405 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance in Colorectal Cancer

Project description:Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance in Colorectal Cancer

| PRJNA573050 | ENA

Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance

Project description:Chip-seq analysis was performed to probe the epigenome related to TGF-β signaling pathway in colorectal cancer

2022-12-01 | GSE141702 | GEO

Histone-acetyl Epigenome Regulates TGF-β Pathway-associated Chemoresistance in Colorectal Cancer

Project description:The global up-regulation of histone acetylation modification after the activation of the TGF-β signaling pathway raised the possibility that the differential expression of specific histone acetyltransferases or histone deacetylases may involve in the modulation of TGF-β-associated chemoresistance in CRC. To test this hypothesis, high-throughput mRNA sequencing (RNA-Seq) was performed to compare the expression profile between SW480 cells treated with or without TGF-β1.

2022-09-01 | GSE137779 | GEO

The TGF-β/SMAD pathway upregulates SRC

Project description:The non-receptor tyrosine kinase SRC is upregulated in various human cancers and plays crucial roles in cancer progression by promoting invasion and metastasis. We show that the transforming growth factor beta (TGF-β/SMAD pathway directly upregulates SRC during the epithelial-mesenchymal transition. In human epithelial MCF10A cells, TGF-β1 treatment markedly upregulated mRNA expression of SRC. Knockout of SMAD4 suppressed upregulation of SRC by TGF-β1. ChIP-sequencing analysis revealed that SRC was transcribed from the SRC1A promoter, which interacted with SMAD2 and SMAD4, in response to TGF-β1. These findings demonstrate that a direct interaction of the activated SMAD complex with the SRC1A promoter directly upregulates SRC and suggest that TGF-β contributes to SRC upregulation in the tumor microenvironment, where TGF-β-mediated tumor progression takes place.

2023-11-20 | GSE122913 | GEO

TGF-β-CTCF regulated pathway

Project description:A TGF-β-CTCF regulated pathway suppresses stem cell associated tumor progression

| PRJEB9452 | ENA

Hypoxic microenvironment activates GLI2 through synergistic action of TGF-β2 and HIF-1α to confer chemoresistance and poor clinical outcome in colorectal cancer [IlluminaExpr_2_CAF_SF_SD208]

Project description:Microenvironment has been suggested as an important factor contributing to how the colorectal cancer cells escape therapy, but the exact mechanism leading to chemoresistance remains elusive. Here, through modeling in vitro by cocultivation of patient-derived cancer associated fibroblasts (CAFs) with cancer stem cells (CSCs), we show that CAFs-secreted TGF-β2 is a key stromal factor that coordinates with hypoxia to promote CSC stemness and resistance to chemotherapy. GLI2, a key transcription factor of Hedgehog pathway, was identified as both necessary and sufficient in this process in which TGF-β and hypoxia-inducible factor (HIF-1α) synergize to directly induce GLI2 expression. Conversely, CSC-secreted TGF-β is also important to support the growth of CAFs but instead induce death of normal fibroblasts, suggesting a reciprocal mechanism to selectively support the CAF-CSC interaction. Small molecule inhibition of both TGF-β and GLI2 effectively reversed the chemoresistance. Finally, expression of TGFB2/HIF1A/GLI2 gene signature as a functional readout of this resistance pathway defines worse clinical outcomes and predicts patients relapse. Our observations uncover a key role of TGF-β/HIF-1α/GLI2 in microenvironment-mediated chemoresistance and reveal novel biomarker and targeting strategies to identify and treat the high risk CRC patients.

2019-01-30 | GSE93254 | GEO

The TGF-β/SMAD pathway upregulates SRC

Project description:The TGF-β/SMAD pathway upregulates SRC

| PRJNA506898 | ENA

Genome wide identification of acetyl-CoA regulated loci

Project description:In order to identify regions of the genome that display quantitative changes in acetyl-CoA, we utilized an established “spike-in” normalization method that allows the quantitative comparison of histone modifications across cell populations using defined quantities of a reference epigenome. We found that some regions of the genome are more sensitive to changes in acetyl-CoA compared to others.

2018-12-20 | GSE109340 | GEO

Ursodeoxycholic acid promoted TGF-β degradation

Project description:MS analysis of proteins interacting with PKA and TGF-β1 in HEK293T cells. MS analysis of immunoprecipitated TGF-β1 in HEK293T cells with TGF-β1 overexpression.

2022-06-28 | PXD031801 | Pride

SIK1 suppresses colorectal cancer metastasis and chemoresistance via the TGF-β signaling pathway.

Project description:In the present study, we investigated the role of salt-induced kinase 1 (SIK1), a serine/threonine kinase protein, in colorectal cancer (CRC). Despite the reported association of SIK1 with tumor malignancy suppression in various cancers, limited research has been conducted on its function in CRC. Our findings revealed that SIK1 expression was low in CRC cells. The results of a KEGG pathway analysis showed a strong association between SIK1 and the TGF-β signaling pathway. In addition, a coimmunoprecipitation assay validated the interaction between SIK1 and Smad7. Our data indicate that SIK1 inhibited the phosphorylation of Smad2, a critical molecule in the Smad-related TGF-β pathway, and downstream target genes of the TGF-β pathway. Furthermore, SIK1 was found to inhibit indicators of epithelial-mesenchymal transition (EMT) and reverse oxaliplatin resistance in CRC. Additionally, SIK1 reduced cell migration and invasion. Our results suggest that the inhibitory effect of SIK1 on the TGF-β pathway contributes to the suppression of metastasis and oxaliplatin chemoresistance in CRC. However, this effect was reversed by galunisertib (LY2157299). In conclusion, our findings provide novel insights into the role of SIK1 in the regulation of the TGF-β pathway in CRC, suggesting its potential as a therapeutic target for the treatment of CRC. Further studies are required to fully characterize the mechanism underlying these observations and to validate these findings in animal models.

| S-EPMC10475365 | biostudies-literature

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