Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA161905 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of human carcinoma-associated fibroblasts (CAFs) comparing control normal fibroblasts (NFs). NFs derived from normal tissues and CAFs derived from the patients with oral cancer were identified by immunocytochemistry. Goal was to determine differentially expressed lncRNAs between NFs and CAFs.
2024-01-08 | GSE164473 | GEO
Project description:180502:
RNA-Sequencing data of cocultured matched CRC patient (P4) derived normal fibroblasts (NFs), cancer associated fibroblasts (CAFs) and tumor spheroids.
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RNA-Sequencing data of cocultured CRC patient derived normal fibroblasts (NFs) or cancer associated fibroblasts (CAFs) (P16, P19, P22, P32, P41, P42) and tumor spheroids (HT29).
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RNA-Sequencing data of IL-1β stimulated fibroblasts (NFs and CAFs)
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RNA-Sequencing of FACS sorted IL1R1 high and IL1R1 low CT5.3 CAFs
| EGAD00001010322 | EGA
Project description:Cancer-associated fibroblasts (CAFs) have been reported to support tumor progression by a variety of mechanisms. However, their role in the progression of non-small cell lung cancer (NSCLC) remains poorly defined. In addition, the extent to which specific proteins secreted by CAFs contribute directly to tumor growth is unclear. To study the role of CAFs in NSCLC, a cross-species functional characterization of mouse and human lung CAFs was performed, including gene expression analysis comparing normal mouse lung fibroblasts (NFs) and mouse lung CAFs to seek for differentially-expressed secreted proteins. Gene expression microarrays were used to identify transcriptomic changes between NFs and CAFs that may contribute to their different tumor-enhancing capacity. NFs and CAFs were grown in vitro for RNA extraction and hybridization on mouse 430_2 Affymetrix microarrays
2013-07-10 | E-GEOD-48397 | biostudies-arrayexpress
Project description:Analysis of gene expression profiles of three cancer-associated fibroblasts (CAFs) and four normal fibroblasts (NFs), which are derived from tumor tissues and adjacent normal mucosa of colorectal cancer patients, respectively.
2019-01-30 | GSE93253 | GEO
Project description:Cancer-associated fibroblasts (CAFs) promote tumor progression through several mechanisms. MicroRNAs (miRNAs) play a key role in CAFs tumor-promoting properties, however, their role in CAFs from different topological areas in lung cancer progression remains unclear. This study aimed to characterize the miRNA expression profile of fibroblasts isolated from matched tumor front (F-CAFs), inner tumor (In-CAFs), and normal adjacent tissue (NFs) in lung adenocarcinoma, using microarray analysis and RT-qPCR. Proliferation and invasion assays of A549 lung cancer cells were performed in the presence of conditioned medium from F-CAFs, In-CAFs and NFs. Pathway enrichment analysis and miRNA-target networks were performed to identify tumorigenesis-related miRNAs. Both F-CAFs and In-CAFs enhanced the proliferation and invasion of A549 cells compared to NFs; however, F-CAFs showed a significantly stronger effect than In-CAFs. qPCR demonstrated three downregulated miRNAs in F-CAFs versus NFs (miR-145-3p, miR-299-3 p, miR-505-3p) and two in F-CAFs versus In-CAFs (miR-410-3p, miR-485-5p). Deregulated miRNAs showed significant association to “pathways in cancer”, “Wnt signaling pathway”, and “TGF-beta signaling pathway”, targeting tumor-promoting growth factors as IGF1 and VEGFA. Our findings suggest that deregulated miRNAs in F-CAFs, which showed the strongest effect on the invasive and proliferative capacity of A546 cancer cells, present potential predictive association with tumor-promoting properties.
2018-04-28 | GSE113805 | GEO
Project description:The tumor microenvironment strongly influences cancer development, progression and metastasis. The role of carcinoma-associated fibroblasts (CAFs) in these processes and their clinical impact has not been studied systematically in non-small cell lung carcinoma (NSCLC). We established primary cultures of CAFs and matched normal fibroblasts (NFs) from 15 resected NSCLC. We demonstrate that CAFs have greater ability than NFs to enhance the tumorigenicity of lung cancer cell lines. Microarray gene expression analysis of the 15 matched CAF and NF cell lines identified 46 differentially expressed genes, encoding for proteins that are significantly enriched for extracellular proteins regulated by the TGF-beta signaling pathway. We have identified a subset of 11 genes that formed a prognostic gene expression signature, which was validated in multiple independent NSCLC microarray datasets. Functional annotation using protein-protein interaction analyses of these and published cancer stroma-associated gene expression changes revealed prominent involvement of the focal adhesion and MAPK signalling pathways. Fourteen (30%) of the 46 genes also were differentially expressed in laser-capture micro-dissected corresponding primary tumor stroma compared to the matched normal lung. Six of these 14 genes could be induced by TGF-beta1 in NF. The results establish the prognostic impact of CAF-associated gene expression changes in NSCLC patients. Methylation profiles of 5 pairs of were included in a molecular characterization of NSCLC fibroblast cell lines (CAFs) vs. normal lung fibroblasts (NFs). Methylation profiles of 5 paired primary NSCLC fibroblast cell lines (CAFs) and normal lung fibroblasts (NFs) were generated. Genes were determined to be hyper- and hypo-methylated based on paired analysis.
2011-04-08 | E-GEOD-27284 | biostudies-arrayexpress
Project description:The tumor microenvironment strongly influences cancer development, progression and metastasis. The role of carcinoma-associated fibroblasts (CAFs) in these processes and their clinical impact has not been studied systematically in non-small cell lung carcinoma (NSCLC). We established primary cultures of CAFs and matched normal fibroblasts (NFs) from 15 resected NSCLC. We demonstrate that CAFs have greater ability than NFs to enhance the tumorigenicity of lung cancer cell lines. Microarray gene expression analysis of the 15 matched CAF and NF cell lines identified 46 differentially expressed genes, encoding for proteins that are significantly enriched for extracellular proteins regulated by the TGF-beta signaling pathway. We have identified a subset of 11 genes that formed a prognostic gene expression signature, which was validated in multiple independent NSCLC microarray datasets. Functional annotation using protein-protein interaction analyses of these and published cancer stroma-associated gene expression changes revealed prominent involvement of the focal adhesion and MAPK signalling pathways. Fourteen (30%) of the 46 genes also were differentially expressed in laser-capture micro-dissected corresponding primary tumor stroma compared to the matched normal lung. Six of these 14 genes could be induced by TGF-beta1 in NF. The results establish the prognostic impact of CAF-associated gene expression changes in NSCLC patients. Genotyping profiles of 4 pairs of were included in a molecular characterization of NSCLC fibroblast cell lines (CAFs) vs. normal lung fibroblasts (NFs). Genotyping profiles of 4 paired primary NSCLC fibroblast cell lines (CAFs) and normal lung fibroblasts (NFs) were generated. CNV was assessed using paired analysis.
2011-04-08 | E-GEOD-27289 | biostudies-arrayexpress
Project description:Cancer-associated fibroblasts (CAFs) are abundantly present in the microenvironment of virtually all tumors and strongly impact tumor progression. Despite increasing insight into their function and heterogeneity, little is known regarding the origin of CAFs. Understanding the origin of CAF heterogeneity is needed to develop successful CAF-based targeted therapies. Through various transplantation studies in mice we determined that CAFs in both invasive lobular breast cancer and triple negative breast cancer originate from mammary tissue-resident normal fibroblasts (NFs). Single-cell transcriptomics, in vivo tracing and in vitro studies revealed the transition of CD26+ and CD26- NF populations into inflammatory CAFs (iCAFs) and myofibroblastic CAFs (myCAFs), respectively. In vitro functional assays showed that CD26+ NFs transition into pro-tumorigenic iCAFs which recruit myeloid cells in a CXCL12-dependent manner and enhance tumor cell invasion via matrix-metalloproteinase (MMP) activity. Together, our data show that CD26+ and CD26- NFs transform into distinct CAF subpopulations in breast cancer.
2022-11-29 | GSE205262 | GEO
Project description:Cancer-associated fibroblasts (CAFs) are abundantly present in the microenvironment of virtually all tumors and strongly impact tumor progression. Despite increasing insight into their function and heterogeneity, little is known regarding the origin of CAFs. Understanding the origin of CAF heterogeneity is needed to develop successful CAF-based targeted therapies. Through various transplantation studies in mice we determined that CAFs in both invasive lobular breast cancer and triple negative breast cancer originate from mammary tissue-resident normal fibroblasts (NFs). Single-cell transcriptomics, in vivo tracing and in vitro studies revealed the transition of CD26+ and CD26- NF populations into inflammatory CAFs (iCAFs) and myofibroblastic CAFs (myCAFs), respectively. In vitro functional assays showed that CD26+ NFs transition into pro-tumorigenic iCAFs which recruit myeloid cells in a CXCL12-dependent manner and enhance tumor cell invasion via matrix-metalloproteinase (MMP) activity. Together, our data show that CD26+ and CD26- NFs transform into distinct CAF subpopulations in breast cancer.
2022-11-29 | GSE205259 | GEO
Project description:Cancer-associated fibroblasts (CAFs) are abundantly present in the microenvironment of virtually all tumors and strongly impact tumor progression. Despite increasing insight into their function and heterogeneity, little is known regarding the origin of CAFs. Understanding the origin of CAF heterogeneity is needed to develop successful CAF-based targeted therapies. Through various transplantation studies in mice we determined that CAFs in both invasive lobular breast cancer and triple negative breast cancer originate from mammary tissue-resident normal fibroblasts (NFs). Single-cell transcriptomics, in vivo tracing and in vitro studies revealed the transition of CD26+ and CD26- NF populations into inflammatory CAFs (iCAFs) and myofibroblastic CAFs (myCAFs), respectively. In vitro functional assays showed that CD26+ NFs transition into pro-tumorigenic iCAFs which recruit myeloid cells in a CXCL12-dependent manner and enhance tumor cell invasion via matrix-metalloproteinase (MMP) activity. Together, our data show that CD26+ and CD26- NFs transform into distinct CAF subpopulations in breast cancer.
2022-11-29 | GSE205223 | GEO