Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human Subperitoneal Fibroblasts and Cancer Cell Interaction Creates Microenvironment Enhancing Tumor Progression and Metastasis

ABSTRACT: Fibroblasts isolated from human colon submucosal and subperitoneal layer were stimulated by colon cancer cell line (DLD-1) cultured medium. Peritoneal invasion in colon cancer is an important prognostic factor, and the fibrosis with α-SMA was a significant pathological feature of the cancer microenvironment formed by peritoneal invasion (CMPI). The result indicated that the gene expression of subperitoneal fibroblasts showed more various gene modification than submucosal fibroblasts. And ACTA2 expression was higher in fibroblasts from subperitoneal layer than that from submucosal layer. Together with this concordant stromal protein expression in CMPI, this in vitro model is able to reflect the special microenvironment in CMPI.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53059 | GEO | 2014/02/20

SECONDARY ACCESSION(S): PRJNA230781

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Human Subperitoneal Fibroblasts and Cancer Cell Interaction Creates Microenvironment Enhancing Tumor Progression and Metastasis

Project description:Fibroblasts isolated from human colon submucosal and subperitoneal layer were stimulated by colon cancer cell line (DLD-1) cultured medium. Peritoneal invasion in colon cancer is an important prognostic factor, and the fibrosis with α-SMA was a significant pathological feature of the cancer microenvironment formed by peritoneal invasion (CMPI). The result indicated that the gene expression of subperitoneal fibroblasts showed more various gene modification than submucosal fibroblasts. And ACTA2 expression was higher in fibroblasts from subperitoneal layer than that from submucosal layer. Together with this concordant stromal protein expression in CMPI, this in vitro model is able to reflect the special microenvironment in CMPI. 3 cases of human colon submucosal and subperitoneal fibroblasts were isolated, and these fibroblasts were stimulated with DLD-1 cultured medium. Total RNA were extracted from these samples and hybridized in Affymetrix microarray to compare their gene expression changes through the DLD-1 stimulation

2014-02-20 | E-GEOD-53059 | biostudies-arrayexpress

The establishment of diagnosis and endoscopic mucosal resection criteria of early colorectal cancer with premalignant lesion in China

Project description:Interventions: Gold Standard:;Index test: Primary outcome(s): Invasion depth of colorectal cancer in submucosal layer;Lymph node metastasis Study Design: Diagnostic test for accuracy

| 2662406 | ecrin-mdr-crc

Global gene expression analysis of human fibroblasts from whole body

Project description:Fibroblasts are the principal stromal cells that exist in whole organs and play vital roles in many biological processes. Although the functional diversity of fibroblasts has been estimated, a comprehensive analysis of fibroblasts from the whole body has not been performed and their phenotypical diversity has not been sufficiently explored. The aim of this study was to elucidate the phenotypical diversity of human fibroblasts within the whole body. Global gene expression analysis of 63 human primary fibroblasts from 13 organs elucidated that fibroblasts from the gastrointestinal tract showed a remarkably distinct character compared to that seen in other organs. Furthermore, gastrointestinal fibroblasts were created by topologically diverse subgroups of fibroblasts depending on their organ and histoanatomical site in the gastrointestinal walls. Global gene expression analysis was performed on 63 human primary fibroblasts from 13 anatomical organs. Of these, 32 fibroblasts from gastrointestinal organs were obtained from a pair of 2 histoanatomical sites, including the submucosal layer (submucosal fibroblasts: SMFs) and subperitoneal layer (subperitoneal fibroblasts: SPFs). Using hierarchical clustering analysis, identifiable phenotypical subgroups of fibroblasts were elucidated and the phenotypical character of each subgroup was analyzed.

2014-11-26 | E-GEOD-63626 | biostudies-arrayexpress

HAPLN1 potentiates peritoneal metastasis in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) frequently metastasizes into the peritoneum, which contributes to poor prognosis. Metastatic spreading is promoted by cancer cell plasticity, yet its regulation by the microenvironment is incompletely understood. Here, we show that the presence of hyaluronan and proteoglycan link protein-1 (HAPLN1) in the extracellular matrix enhances tumor cell plasticity and PDAC metastasis. Bioinformatic analysis showed that HAPLN1 expression is enriched in the basal PDAC subtype and associated with worse overall patient survival. In a mouse model for peritoneal carcinomatosis, HAPLN1-induced immunomodulation favored a more permissive microenvironment, which accelerated the peritoneal spread of tumor cells. Mechanistically, HAPLN1, via upregulation of tumor necrosis factor receptor 2 (TNFR2), promoted TNF-mediated upregulation of Hyaluronan (HA) production, facilitating EMT, stemness, invasion and immunomodulation. Extracellular HAPLN1 modified cancer cells and fibroblasts, rendering them more immunomodulatory. As such, we identified HAPLN1 as a prognostic marker and as a driver for peritoneal metastasis in PDAC.

2023-03-31 | GSE211126 | GEO

Heat Shock Factor 1-dependent extraceHeat Shock Factor 1-dependent extracellular matrix remodeling mediates the transition from chronic intestinal inflammation to colon cancerllular matrix remodeling mediates the transition from chronic intestinal inflammation to colon cancer

Project description:Chronic inflammation underlies tumor initiation, progression, invasion, and metastasis. In the colon, long-term exposure to chronic inflammation drives colitis associated colon cancer (CAC) in patients with inflammatory bowel disease (IBD). While the causal and clinical links between chronic inflammation and CAC are well established, our molecular understanding of how chronic inflammation leads to the development of colon cancer is still lacking. Here we deconstruct the evolving microenvironment of CAC, by measuring proteomic changes and extracellular matrix (ECM) organization over time in a genetically modified mouse model of CAC. We detect early changes in ECM structure and composition, and report that the transcriptional regulator heat shock factor 1 (HSF1) plays a crucial role in orchestrating these events. Activated in stromal fibroblasts of the gut, HSF1 promotes ECM remodeling and inflammatory programs which lead to the development of CAC. Loss of HSF1 abrogates ECM assembly by colon fibroblasts in cell culture, prevents inflammation-induced ECM remodeling in mice and significantly inhibits progression to CAC. Establishing the relevance of our experimental findings to human disease, we find high activation of stromal HSF1 in CAC patients, and detect the HSF1-dependent proteomic ECM signature in human colorectal cancer. Thus, HSF1-dependent ECM remodeling plays a crucial role in mediating inflammation-driven colon cancer.

2020-11-05 | PXD022207 | Pride

Methylome and transcriptome sequencing to study epigenetic alterations in colon associated fibroblasts from normal, colitis and cancer associated fibroblasts

Project description:The colon cancer associated fibroblasts are part of the tumor microenvironment and has been shown to facilitate colon cancer progression by secretion of various signaling molecules and growth hormones. Similarly, the fibroblasts associated with colitic colons secrete pro-inflammatory cytokines that promote inflammation of the colon. However, the molecular mechanisms that underlie these gene expression changes in these fibroblasts is unclear. To characterize the epigenetic mechanisms that may contribute to the gene expression changes in these fibroblasts, we performed RNA-seq and MBD-isolated genome sequencing (MiGS or MBD-seq) on colon associated fibroblasts isolated from normal, colitis and cancer patients.

2022-12-29 | GSE92945 | GEO

Gene expression analysis of M and SM gastric cancer

Project description:The objective of this study was to identify genes and pathways involved in submucosal invasion of early gastric cancer through comprehensive gene expression analysis.

2023-12-22 | GSE208099 | GEO

Expression data from human pancreatic ductal adenocarcinomas by stroma types

Project description:Pancreatic cancer is characterized by abundant desmoplastic stroma. Despite numerous theoretical and experimental efforts, therapeutic approaches targeting pancreatic cancer stroma have been largely unsuccessful, highlighting the need for more comprehensive assessment of inter- and intratumoral stromal heterogeneity in a large series of clinical tumors. Quantitative computation of FAP-dominant fibroblasts, ACTA2-dominant fibroblasts, and intratumoral collagen in whole-tissue sections from 215 treatment-naïve pancreatic cancers allowed us to identify three distinct stroma types (FAP-dominant fibroblast-rich stroma [F-stroma], ACTA2-dominant fibroblast-rich stroma [A-stroma], and collgen-rich stroma [C-stroma]), which were differentially associated with patient outcomes, molecular characteristics and the immunosuppressive tumor microenvironment. We explored differentially expressed genes between three distinct stroma types (F-stroma, A-stroma, and C-stroma) using frozen samples from 20 patients with pancreatic cancer.

2020-09-03 | GSE157353 | GEO

Sphingosine kinase 2 in stromal fibroblasts creates a hospitable tumor microenvironment in breast cancer

Project description:Reciprocal interactions between breast cancer cells and the tumor microenvironment are important for cancer progression and metastasis. We report here that the deletion or inhibition of sphingosine kinase 2 (SphK2), which produces sphingosine-1-phosphate (S1P), markedly suppresses syngeneic breast tumor growth and lung metastasis in mice by creating a hostile microenvironment for tumor growth and invasion. SphK2 deficiency decreased S1P and concomitantly increased ceramides, including C16-ceramide, in stromal fibroblasts. Ceramide accumulation suppressed activation of cancer-associated fibroblasts (CAFs) by upregulating stromal p53, which restrained production of tumor-promoting factors to reprogram the tumor microenvironment and restrict breast cancer establishment. Ablation of p53 in SphK2-deficient fibroblasts reversed these effects, enabled CAF activation and promoted tumor growth and invasion. These data uncovered a novel role of SphK2 in regulating non-cell autonomous functions of p53 in stromal fibroblasts and their transition to tumor-promoting CAFs, paving the way for the development of a strategy to target the tumor microenvironment and enhance therapeutic efficacy.

2020-01-01 | GSE136655 | GEO

microRNA-143 downregulates Hexokinase 2 in colon cancer cells

Project description:MicroRNAs (miRNAs) have emerged as important gene regulators and are recognized as key players in tumorigenesis. miR-143 is reported to be down-regulated in several cancers, but knowledge of its targets in colon cancer remains limited. To investigate the role of miR-143 in colon cancer, we have employed a microarray based approach to identify miR-143 targets. Based on seed site enrichment analyses and unbiased word analyses, we found a significant enrichment of miRNA binding sites in the 3M-bM-^@M-^Y-untranslated regions (UTRs) of transcripts down-regulated upon miRNA overexpression. Here we identify Hexokinase 2 (HK2) as a direct target of miR-143 and show that re-introduction of miR-143 in the colon cancer cell line DLD-1 results in a decreased lactate secretion, indicating that miR-143 down-regulation of HK2 affects glucose metabolism in colon cancer cells. DLD-1 cells were transfected with 50 nM miR-143 duplex or mock transfected. Total RNA was harvested 24 hours post-transfection and analyzed on Affymetrix HG-U133 Plus 2.0 human arrays.

2012-05-01 | E-GEOD-33420 | 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