Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of IL-6/Jak/STAT3 axis as a specific communicator between gastric cancer-associated fibroblast and gastric cancer cells

ABSTRACT: To identify CAF-specific secreted molecules, we performed transcriptome analysis to compare gene expression patterns between paired NAFs and CAFs isolated from one GC patient.

ORGANISM(S): Homo sapiens

PROVIDER: GSE112350 | GEO | 2021/03/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Twist1 knockdown in two gastric cancer-associated fibroblast lines

Project description:Primary human gastric cancer-associated fibroblast (CAF) cultures (CAF14 and CAF32) were establised from 2 gastrectomy specimens. Silencing the expression (loss-of-function effect) of Twist1 in CAFs showed candidate target genes regulated by Twist1 and abrogated their tumor-promoting properties. Experiment design: two gastric CAFs (CAF14 adn CAF32, respectively) were establised from two gastric cancer patients and Twist1 knockdown studies were performed using shRNA.

2014-10-28 | E-GEOD-62738 | biostudies-arrayexpress

Targeting the IL-6/JAK/STAT3 signalling axis in cancer.

Project description:The IL-6/JAK/STAT3 pathway is aberrantly hyperactivated in many types of cancer, and such hyperactivation is generally associated with a poor clinical prognosis. In the tumour microenvironment, IL-6/JAK/STAT3 signalling acts to drive the proliferation, survival, invasiveness, and metastasis of tumour cells, while strongly suppressing the antitumour immune response. Thus, treatments that target the IL-6/JAK/STAT3 pathway in patients with cancer are poised to provide therapeutic benefit by directly inhibiting tumour cell growth and by stimulating antitumour immunity. Agents targeting IL-6, the IL-6 receptor, or JAKs have already received FDA approval for the treatment of inflammatory conditions or myeloproliferative neoplasms and for the management of certain adverse effects of chimeric antigen receptor T cells, and are being further evaluated in patients with haematopoietic malignancies and in those with solid tumours. Novel inhibitors of the IL-6/JAK/STAT3 pathway, including STAT3-selective inhibitors, are currently in development. Herein, we review the role of IL-6/JAK/STAT3 signalling in the tumour microenvironment and the status of preclinical and clinical investigations of agents targeting this pathway. We also discuss the potential of combining IL-6/JAK/STAT3 inhibitors with currently approved therapeutic agents directed against immune-checkpoint inhibitors.

| S-EPMC5858971 | biostudies-literature

Twist1 knockdown in two gastric cancer-associated fibroblast lines

2014-10-28 | GSE62738 | GEO

Hypoxia-induced proteomic remodeling of human mammary cancer associated fibroblast

Project description:Intratumoral hypoxia causes the formation of dysfunctional blood vessels which contribute to tumor metastasis. Blood vessels are embedded in the tumor stroma where cancer-associated fibroblasts (CAFs) constitute the most prominent cellular component. We found that hypoxic human mammary CAFs promote blood vessel growth in CAF-endothelial cell co-cultures in vitro. Mass spectrometry-based proteomic analysis of CAF secretome unravels how hypoxic CAFs contribute to blood vessel abnormalities by altering the secretion of a multitude of pro- and anti-angiogenic factors. Hypoxia induces pronounced remodeling of the CAF proteome, including proteins that have not been previously related to this process. Our study provides a map of unprecedented depth of hypoxia-induced molecular alterations in mammary CAFs that can be exploited to identify novel mechanisms that control hypoxic CAF functions.

2019-02-15 | PXD006535 | Pride

STAT3 induces breast cancer growth and progression via IL-6, STC1 and MMP13 secretion by Cancer Associated Fibroblasts

Project description:In the tumor microenvironment, Cancer Associated Fibroblasts (CAFs) become activated by cancer cells and increase their secretory activity to produce soluble factors that contribute to tumor cells proliferation, invasion and dissemination to distant organs. The pro-tumorigenic transcription factor STAT3 and its canonical inducer, the pro-inflammatory cytokine IL-6 act conjunctly in a positive feedback loop that maintains high levels of IL-6 secretion and STAT3 activation in both tumor and stromal cells. Here, we demonstrate that STAT3 is essential for the pro-tumorigenic functions of murine breast cancer CAFs both in vitro and in vivo, and identify a STAT3 signature significantly enriched for genes encoding for secreted proteins. Among those, IL-6, ANGPTL4, STC-1 and MMP13 were validated as STAT3-dependent mediators of CAF pro-tumorigenic functions by different approaches. CAFs activities were moreover impaired by IL-6 Receptor blocking antibodies and by MMP13 inhibition, supporting the feasibility of a therapeutic approach based on inhibiting STAT3-induced CAF-secreted proteins. The usefulness of such an approach is supported by the observation that an equivalent CAF-STAT3 signature in humans is expressed at high levels in breast cancer stromal cells and characterizes patients with a shorter disease specific survival, including those with basal-like disease.

2021-12-31 | GSE178081 | GEO

Hypoxia-induced proteomic remodeling of human mammary cancer associated fibroblast - siRNA NCBP2-AS2

Project description:Intratumoral hypoxia causes the formation of dysfunctional blood vessels which contribute to tumor metastasis. Blood vessels are embedded in the tumor stroma where cancer-associated fibroblasts (CAFs) constitute the most prominent cellular component. We found that hypoxic human mammary CAFs promote blood vessel growth in CAF-endothelial cell co-cultures in vitro. Mass spectrometry-based proteomic analysis of CAF secretome unravels how hypoxic CAFs contribute to blood vessel abnormalities by altering the secretion of a multitude of pro- and anti-angiogenic factors. Hypoxia induces pronounced remodeling of the CAF proteome, including proteins that have not been previously related to this process. Amongst those, the uncharacterized antisense gene protein NCBP2-AS2 is one of the most transcriptionally upregulated proteins in the proteome and secretome of hypoxic CAFs. Silencing of NCBP2-AS2 abrogates the pro-angiogenic function acquired by hypoxic CAFs through decreasing VEGF expression levels to the levels found in normoxic CAFs.

2019-02-15 | PXD006539 | Pride

The transcriptome profile of the stomach fibroblasts with high-metastatic or low-metastatic gastric cancer cell-derived extracellular vesicles.

Project description:Cancer-associated fibroblasts (CAFs) have an important role in the tumor progression. CAFs are heterogeneous, and its subpopulation with distinct functions have been regarded as the major obstacle to CAF targeting therapy. However, it is still unclear how cancer cells mediate CAF subpopulations and create preferable tumor microenvironment for their metastasis. In this study, by using the metastatic cancer cell line models of diffuse-type gastric cancer (DGC), we demonstrate that high-metastatic cancer cell-derived extracellular vesicles (EVs) contribute to the formation of activated fibroblast subpopulations. High-metastatic DGC cells create at least two types of CAF subpopulations: myofibroblastic feature and chemokine producing feature. The CAF subpopulation with chemokine producing feature was selectively induced by high-metastatic DGC cell-derived EVs. We also found that high-metastatic DGC cell-derived EVs contain various miRNAs to induce chemokine expression in the fibroblasts. Our findings suggest that intercellular communications via EVs contribute to establishing the appropriate tumor microenvironment toward cancer metastasis. To study the effect of EVs derived from GC cell lines on gene expression in the stomach fibroblasts, transcriptome analysis for the stomach fibroblasts with EVs derived from GC cell lines was performed.

2019-03-31 | GSE116176 | GEO

Cancer-associated fibroblast-secreted FGF2 faliciates gastric cancer cell proliferation by enhancing ribosome biogenesis

Project description:Cell co-culture experiments and bioinformatics analysis show that soluble FGF2 plays an important role in the cross-talking between CAF and tumor cells. This study aimed to explore the efffects of human recombinant FGF2 protein (20 ng/mL) on the transcriptome of GC cells.

2024-03-14 | GSE249966 | GEO

Distinct fibroblast functional states drive clinical outcomes in ovarian cancer and are regulated by TCF21

Project description:Recent studies indicate that cancer-associated fibroblasts (CAFs) are phenotypically and functionally heterogeneous. However, little is known about CAF subtypes and the roles they play in cancer progression. Here we identify and characterize two CAF subtypes that coexist within high grade serous ovarian cancers: Fibroblast activation protein (FAP)-high (FH) CAFs resemble the classical myofibroblast-type CAF, whereas FAP-low (FL) CAFs possesses a preadipocyte-like molecular signature.

2020-05-01 | GSE126132 | GEO

Distinct fibroblast functional states drive clinical outcomes in ovarian cancer and are regulated by TCF21

2020-05-01 | GSE126131 | GEO