ITGA11 expression of CAF promotes tumorigenicity and metastasis in NSCLC
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE51722
PROVIDER: PRJNA229136 | ENA |
REPOSITORIES: ENA
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Project description:Integrin alpha-11-beta-1 is stroma specific receptor for fibrillar collagen, as it is mainly over-expressed in carcinoma-associated fibroblasts (CAFs). However, its direct role in cancer progression remains unclear. We have investigated this role by generating severe combined immune deficient (SCID) mice deficient in integrin alpha-11 (alpha-11) expression. The growth of A549 lung adenocarcinoma cells in integrin alpha-11 knockout animals (alpha-11-/-) was significantly impeded, as compared to wild type (alpha-11+/+) SCID mice. Orthotopic implantation of a spontaneously metastatic NCI-H460SM cells into the lungs of alpha-11-/- and alpha-11+/+ mice showed significant reduction in the metastatic potential of these cells in the alpha-11 deficient mice. Our data support an important role for alpha-11 signaling pathway in CAFs, promoting tumor growth and metastatic potential of non-small cell lung cancer (NSCLC) cells by regulating the expression of alpha-SMA and stromal collagen-cross linking genes as the latter affects the organization and stiffness of fibrillar collagen.
2015-07-15 | GSE51722 | GEO
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Project description:The cellular diversity of stromal compartment within the tumor microenvironment might change dynamically as tumors evolve that allowing distant dissemination of tumor cells and informing the treatment options. We used single cell RNA sequencing (scRNA-seq) to provide a detailed insight of cellular components feature in bladder cancer and identify that PDGFRα+ITGA11+ CAFs were essential for lymphatic metastasis of bladder cancer. To identify molecular mechanism of PDGFRα+ITGA11+ CAFs formation, next generation sequencing (NSG) was performed to explore the upregulated genes in bladder cancer-induced PDGFRα+ITGA11+ CAFs.
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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. 30 samples: 15 primary NSCLC fibroblast cell lines, 15 normal lung fibroblast cell lines
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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. 30 samples: 15 primary lung tumor stroma, 15 normal lung parenchyma
2011-04-08 | E-GEOD-22863 | 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. 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.
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Project description:Pleural dissemination in non-small cell lung cancer (NSCLC) refers to the direct spread of cancer cells from the primary tumor site to the extrapulmonary thoracic cavity, where they colonize the pleura. This study aimed to investigate the impact of cancer-associated fibroblasts (CAFs) on the development of pleural dissemination in NSCLC. Through in vitro co-culture and in vivo pleural dissemination models, we identified that CAFs promote cancer cell migration, anchorage-independent growth, adhesion, invasion, and spheroid formation of cancer cells, leading to the development of pleural dissemination. RNA sequencing analysis revealed that CAFs upregulated the expression of Cellular Communication Network Factor 1 (CCN1), a matricellular protein, in cancer cells.
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