Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The CTCF/LncRNA-PACERR/EP300 complex in TAMs promotes the malignant progression of pancreatic ductal adenocarcinoma (PDAC) by docking at the PTGS2 promoter region

ABSTRACT: The CTCF/LncRNA-PACERR/EP300 complex in TAMs promotes the malignant progression of pancreatic ductal adenocarcinoma (PDAC) by docking at the PTGS2 promoter region

PROVIDER: PRJNA716651 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14048934_1.fastq.gz	Fastqsanger.gz
	SRR14048934_2.fastq.gz	Fastqsanger.gz
	SRR14048935_1.fastq.gz	Fastqsanger.gz
	SRR14048935_2.fastq.gz	Fastqsanger.gz
	SRR14048936_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 44

Similar Datasets

The CTCF/LncRNA-PACERR/EP300 complex in TAMs promotes the malignant progression of pancreatic ductal adenocarcinoma (PDAC) by docking at the PTGS2 promoter region

Project description:The unregulated expression of COX-2 in tams is causally related to the occurrence, development and outcome of pancreatic ductal adenocarcinoma. We describe a new basic level of transcriptional control of COX-2 expression. Constructing in vivo and in vitro TAM model lines, we found that CTCF plays a significant role in the chromatin remodeling of pancreatic cancer-related macrophages, and showed that CTCF, which acts as both a transcription factor and an insulator, establishes an open chromatin domain, and Induced the expression of LncRNA PACERR in the upstream promoter region of PTGS2. The newly transcribed LncRNA PACERR binds to the RNA binding region of CTCF to play a cis-regulatory role. The formation of CTCF/LncRNA PACERR complex contributes to the recruitment of EP300 histone acetylation transfer, which increases the global scope of histone acetylation and induces the expression of PTGS2. Our findings reveal that CTCF and LncRNA that was regulated by CTCF at the same position work together to form a complex of CTCF/LncRNA PACERR/EP300 and dock in the PTGS2 promoter region to mediate the unexpected mechanism of PTGS2 expression. And LncRNA PACERR as a new potential target for regulating the malignant progression of pancreatic cancer.

2021-06-30 | GSE169451 | GEO

mRNA profiling of schwann cells cultured with monocytes derived macrophages and PDAC cell lines supernants-induced tumor-associated macrophages (TAMs)

Project description:Tumor associated macrophages(TAMs) have been demonstrated to promote tumor progression and perineural invasion in PDAC, however the underlying machanism of TAMs interacting with Schwann cells is still unclear. We found the gene expression of Schwann cell is different from TAMs-induced Schwann cells by comparing mRNA profiling.

2023-12-20 | GSE194205 | GEO

EP300 promotes ferroptosis via HSPA5 acetylation in pancreatic cancer

Project description:Ferroptosis is a form of regulated cell death characterized by oxidative injury-induced lipid peroxidation. However, the detailed protein post-translational modification regulatory mechanism of ferroptosis remains largely unknown. Here, we report that E1A binding protein P300 (EP300) acetyltransferase promotes ferroptosis in human pancreatic ductal adenocarcinoma (PDAC) cells via the acetylation of heat shock protein family A (Hsp70) member 5 (HSPA5, also known as GRP78 or BIP) on the site of K353. Acetylated HSPA5 loses its ability to inhibit lipid peroxidation and subsequent ferroptotic cell death. Genetic or pharmacological inhibition of EP300-mediated HSPA5 acetylation on K353 increases PDAC cell resistance to ferroptosis. Moreover, histone deacetylase 6 (HDAC6) limits HSPA5 acetylation and subsequent ferroptosis.

2023-10-24 | PXD039998 | Pride

Differential gene expression analysis of PTGS2-inducing and PTGS2-non-inducing oropharyngeal carcinoma cell lines.

Project description:Prostaglandin E2 (PGE2) is a powerful immunomodulator synthesized by the COX2 enzyme, coded by human gene PTGS2. PGE2 is known to possess angiogenic, protumor and immunosuppressive functionality in the microenviornment of oropharyngeal carcinomas (OPC). Differential induction of PTGS2 in infiltrating myeloid-derived immunocytes has been observed with media conditioned by cultured OPC biopsies and OPC-derived cell lines alike. To identify PTGS2-inducing, OPC-derived gene products, we utilized bluk RNA sequencing on 4 OPC-derived cell lines to compare expression profiles of PTGS2-inducing (SCC154, SCC25) with that of PTGS2-non-inducing (2A3, SCC152) cell lines. Interleukin-1α (IL-1α) was among the differentially expressed candidates between cell lines.

2022-10-21 | GSE215973 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - scRNAseq of human PDAC samples

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with high resistance to therapy. Inflammatory and immunomodulatory signals co-exist in the tumor microenvironment (TME), leading to dysregulated reparative and cytotoxic responses. Tumor-associated macrophages (TAMs) control immune dynamics in the TME, but their heterogeneity and plasticity have hampered understanding of the underlying mechanisms. Here, we combined single-cell and spatial genomics with functional experiments to elucidate macrophage functions in PDAC. We uncovered an inflammatory loop between tumor cells and interleukin (IL)-1b+ TAMs, a subset of macrophages elicited by a local synergy between prostaglandin E2 (PGE2) and tumor necrosis factor (TNF)-a. Interfering with the PGE2-IL-1b axis elicited TAM reprogramming and antagonized tumor-intrinsic inflammation, leading to PDAC control in vivo. IL-1b+ TAMs are conserved across human cancers and correlate with inflammation and patient prognosis in a context-dependent manner. Our study highlights how TAMs govern between inflammation and immune suppression in cancer, with significant therapeutic implications.

2023-09-11 | GSE217845 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - Molecular Cartography of human PDAC samples

2023-09-11 | GSE237846 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - scRNA-seq of murine PDAC samples

2023-09-11 | GSE217846 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - Spatial transcriptomics of mouse PDAC samples

2023-09-11 | GSE217843 | GEO

mRNA profiling of monocytes derived macrophages and PDAC cell lines supernants-induced tumor-associated macrophages (TAMs)

Project description:mRNA profiling of monocytes derived macrophages and PDAC cell lines supernants-induced tumor-associated macrophages (TAMs)

| PRJNA799382 | ENA

Gene expression profiles of tumor-associated macrophages (TAMs) overexpressing miR-511-3p

Project description:Hematopoietic stem/progenitor cells (HS/PCs) were transduced with lentiviral vectors overexpressing OFP and either miR-511-3p or a control, mutated miRNA sequence (miR-511-3p-mut). The transduced HS/PCs were then transplanted in recipient C57BL/6 mice. Tumors (Lewis lung carcinomas, LLC) were injected s.c. 4 weeks after HS/PC transplant. Lentiviral vector-transduced (OFP+), tumor-associated macrophages (TAMs) were isolated 4 weeks after LLC injection by fluorescence-activated cell sorting. Gene expression profiles of TAMs overexpressing either miR-511-3p or miR-511-3p-mut were obtained from 3 independent biological samples/each. Gene expression profiles of miRNA-overexpressing TAMs were then compared with the gene expression profiles of wild-type TAMs isolated from LLCs grown in nontransplanted C57BL/6 mice; the latter TAMs were subfractioned into MRC1+CD11c(low) or CD11c+MRC1(low) subsets before RNA isolation and analysis. Comparison of gene expression profiles of TAMs revealed that miR-511-3p overexpression tunes down the expression of multiple genes that are classically upregulated in protumoral MRC1+CD11c(low) TAMs. TAMs were isolated from Lewis lung carcinomas grown s.c. in C57BL/6 mice.

2012-04-01 | E-GEOD-34903 | 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