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MicroRNA expression in prostate cancer cells stimulated with cancer associated fibroblasts

ABSTRACT: Tumor microenvironment is a strong determinant for the acquisition of metastatic potential of cancer cells. It has been demonstrated (Giannoni E et al., Cancer Res 2010) that cancer associated fibroblasts (CAF) elicit an epithelial-mesenchymal transition (EMT) in prostate cancer (PCa) cells, leading to enhanced tumor cell aggressiveness. Here, we investigated the involvement of microRNAs (miRNA) in such malignant tumor-stroma interplay, to identify possible tools to counteract metastasis dissemination.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42699 | GEO | 2013/09/01

SECONDARY ACCESSION(S): PRJNA182757

REPOSITORIES: GEO

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MicroRNA expression in prostate cancer cells stimulated with cancer associated fibroblasts

Project description:Tumor microenvironment is a strong determinant for the acquisition of metastatic potential of cancer cells. It has been demonstrated (Giannoni E et al., Cancer Res 2010) that cancer associated fibroblasts (CAF) elicit an epithelial-mesenchymal transition (EMT) in prostate cancer (PCa) cells, leading to enhanced tumor cell aggressiveness. Here, we investigated the involvement of microRNAs (miRNA) in such malignant tumor-stroma interplay, to identify possible tools to counteract metastasis dissemination. To verify whether specific miRNAs are involved in CAF-induced EMT in PCa cells, PC-3 cells were subjected to a variety of stimuli, known to induce or not the acquisition of a mesenchymal phenotype (Giannoni E et al., Cancer Res 2010; Giannoni E et al., Antioxid Redox Signal 2011) , and profiled for miRNA expression on a microarray platform. miRNA expression profiles successfully distinguished cells that underwent EMT following the stimulation with activated fibroblasts (here referred to as “mesenchymal”) from cells that did not (“epithelial”).

2013-09-01 | E-GEOD-42699 | biostudies-arrayexpress

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

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. Because the CAF subpopulations are likely depending on the cancer cell subtypes and aggressiveness, it is conceivable the possibility that high-metastatic cancer cells have the capacity to induce the appropriate CAF subpopulation compared with low-metastatic cancer cells. To make it clear, by using the metastatic cancer cell line models of diffuse-type gastric cancer (DGC), we cultured the immortalized stomach fibroblasts with high-metastatic and low-metastatic DGC cell lines. And then, we compared the transcriptome profile of them by microarray analysis. It has shown that high-metastatic DGC cells can induce at least two types of CAF-like phenotypes: myofibroblastic feature and chemokine producing feature. We also found that these two features of fibroblasts were basically distributed in the different fibroblasts. These data indicated that high-metastatic DGC cells form the distinct CAF subpopulations.

2019-03-31 | GSE116167 | GEO

Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 1: Proteins transferred from cancer-associated fibroblasts to endothelial cells : trans-SILAC)

Project description:Intercellular communication between different cell types in solid tumors contributes to tumor growth and metastatic dissemination. The secretome of cancer-associated fibroblasts (CAFs) plays major roles in these processes. Using human mammary CAFs, we unveil a mechanism of cell-cell communication between CAFs with a myofibroblast phenotype and endothelial cells (ECs) based on intercellular protein transfer through extracellular vesicles (EVs). CAFs transfer proteins to ECs, including plasma membrane receptors, which we have identified by using mass spectrometry-based proteomics. Using THY1 as an example of transferred plasma membrane-bound protein, we show that CAF-derived proteins can influence how ECs interact with other cell types. Here, we show that CAFs produce high amounts of matrix-bound EVs that have a key role in protein transfer. Hence, our work paves the way for further studies to understand how CAF-derived matrix-bound EVs influence tumor pathology by regulating functions of neighboring cancer, stromal and immune cells.

2024-02-16 | PXD034450 | Pride

Bidirectional crosstalk between cancer cells and cancer-associated fibroblasts in mixed organoid system elicits transcriptomic characteristics of pancreatic cancer with potential therapeutic vulnerabilities [scRNA-seq]

Project description:Pancreatic cancer's aggressiveness and poor response to conventional treatment have long necessitated a personalized medicine platform. Patient-derived pancreatic cancer organoids (PCOs) with matching genetic mutations have emerged as valuable tools for drug screening. However, PCOs, composed solely of cancer cells, may exhibit different characteristics from the original tumors due to the absence of the tumor microenvironment (TME). To address these issues, we extensively characterized the transcriptomic features of matched patient-derived mixed PCO-CAF systems, combining pancreatic cancer cells and cancer-associated fibroblasts (CAFs), compared to PCOs and the original tumors. The mixed PCO-CAF model closely resembled the patient tissue's transcriptomic traits, indicating its potential in reflecting the TME. Single-cell RNA sequencing revealed different cell populations in the mixed PCO-CAF system, including myofibroblast-like CAFs and inflammatory CAFs, influencing the essential features of cancer cells in the TME. Several growth factors and cytokines were identified in both the patient tissue and mixed PCO-CAFs, suggesting the importance of intercellular signaling communication. Importantly, disrupting these interactions could lead to antitumor responses. Given the cumulative implications of our dataset, the mixed PCO-CAF emerges as a clinically applicable paradigm for personalized therapeutics.

2024-02-28 | GSE253559 | GEO

2024-02-28 | GSE253558 | GEO

Cancer-associated fibroblasts rewire the estrogen receptor response in luminal breast cancer, enabling estrogen independence

Project description:Advanced breast cancers represent a major therapeutic challenge due to their refractoriness to treatment. Cancer-associated fibroblasts (CAFs) are the most abundant constituents of the tumor microenvironment and have been linked to most hallmarks of cancer. However, the influence of CAFs on therapeutic outcome remains largely unchartered. Here, we reveal that spatial coincidence of abundant CAF infiltration with malignant cells was associated with reduced estrogen receptor (ER)-α expression in luminal breast tumors. Notably, CAFs mediated estrogen-independent tumor growth by selectively regulating ER-α signaling. Whereas most prototypical estrogen-responsive genes were suppressed, CAFs maintained gene expression related to therapeutic resistance. A high-throughput drug screen in co-cultures identified effector pathways involved in the CAF-induced regulation of ER-α signaling. Among these, the transforming growth factor-β and the janus kinase signaling cascades were validated as actionable targets to counteract the CAF-induced ER-α modulation. Finally, genes that were downregulated in cancer cells by CAFs were predictive of poor response to endocrine treatment. In conclusion, our work reveals that CAFs directly control the luminal breast cancer phenotype by selectively modulating ER-α expression and transcriptional function, and further proposes novel targets to disrupt the crosstalk between CAFs and tumor cells to reinstate treatment response to endocrine therapy in patients.

2024-02-23 | GSE251644 | GEO

Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 5: pCAF1 proteome)

2024-02-16 | PXD034573 | Pride

Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 6: Mammary Fibroblasts Proteome)

2024-02-16 | PXD049116 | Pride

Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 2: THP-1 proteome )

2024-02-16 | PXD034460 | 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

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