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Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 1]

ABSTRACT: Stromal communication with cancer cells can influence treatment response. We show that stromal and breast cancer (BrCa) cells utilize paracrine and juxtacrine signaling to drive chemotherapy and radiation resistance. Upon heterotypic interaction, exosomes are transferred from stromal to BrCa cells. RNA within exosomes, which are largely non-coding transcripts and transposable elements, stimulates the pattern recognition receptor RIG-I to activate STAT1-dependent anti-viral signaling. In parallel, stromal cells also activate NOTCH3 on BrCa cells. The paracrine anti-viral and juxtacrine NOTCH3 pathways converge as STAT1 facilitates transcriptional responses to NOTCH3 and expands therapy resistant tumor-initiating cells. Primary human and/or mouse BrCa analysis support the role of anti-viral/NOTCH3 pathways in NOTCH signaling and stroma-mediated resistance, which is abrogated by combination therapy with gamma secretase inhibitors. Thus, stromal cells orchestrate an intricate cross-talk with BrCa cells by utilizing exosomes to instigate anti-viral signaling. This expands BrCa subpopulations adept at resisting therapy and re-initiating tumor growth. Breast cancer cells lines and MRC5 fibroblasts were mono-cultured or co-cultured together. Cell types were separated by FACS and gene expression changes were examined using the Affymetrix Human Gene 1.0ST arrays. The effect of tumor-stromal cell interaction on different breast cancer cell types was analyzed using biological replicates. Gene expression changes resulting from knockdown of STAT1 was also investigated.

ORGANISM(S): Homo sapiens

SUBMITTER: Andy Minn

PROVIDER: E-GEOD-60994 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 2]

Project description:Stromal communication with cancer cells can influence treatment response. We show that stromal and breast cancer (BrCa) cells utilize paracrine and juxtacrine signaling to drive chemotherapy and radiation resistance. Upon heterotypic interaction, exosomes are transferred from stromal to BrCa cells. RNA within exosomes, which are largely non-coding transcripts and transposable elements, stimulates the pattern recognition receptor RIG-I to activate STAT1-dependent anti-viral signaling. In parallel, stromal cells also activate NOTCH3 on BrCa cells. The paracrine anti-viral and juxtacrine NOTCH3 pathways converge as STAT1 facilitates transcriptional responses to NOTCH3 and expands therapy resistant tumor-initiating cells. Primary human and/or mouse BrCa analysis support the role of anti-viral/NOTCH3 pathways in NOTCH signaling and stroma-mediated resistance, which is abrogated by combination therapy with gamma secretase inhibitors. Thus, stromal cells orchestrate an intricate cross-talk with BrCa cells by utilizing exosomes to instigate anti-viral signaling. This expands BrCa subpopulations adept at resisting therapy and re-initiating tumor growth. Breast cancer cells lines and MRC5 fibroblasts were mono-cultured or co-cultured together. Cell types were separated by FACS and gene expression changes were examined using the Affymetrix Human Gene 1.0ST arrays. The effect of tumor-stromal cell interaction on different breast cancer cell types was analyzed using biological replicates. Gene expression changes resulting from knockdown of STAT1 was also investigated.

2014-10-24 | E-GEOD-60995 | biostudies-arrayexpress

Analysis of exosome RNA from co-culture of cancer cell and stroma cell

Project description:How stroma communicates with cancer to influence treatment response is poorly understood. We show that stromal fibroblasts protect breast cancer (BrCa) against radiation and chemotherapy through an exosome-mediated anti-viral pathway and NOTCH3. Stroma increases RAB27B and transfers exosomes to BrCa. RNA within exosomes, comprised largely of non-coding transcripts and transposable elements, stimulates the pattern recognition receptor RIG-I through a 5M-bM-^@M-^Y-triphosphate motif to activate STAT1. BrCa NOTCH3 is activated in parallel by stromal JAG1 and cooperates with STAT1 to enhance transcriptional responses of NOTCH target genes and to expand therapy resistant tumor-initiating cells. Computational modeling using primary human and mouse BrCa supports the interaction of anti-viral/NOTCH3 pathways in controlling NOTCH target genes and treatment resistance, particularly in basal subtype tumors. Gamma secretase inhibitors reverse stromal protection and abrogate radiation resistance in vivo. Thus, stroma orchestrates an intricate cross-talk with BrCa by utilizing exosomes to coax anti-viral signaling that expands therapy resistant cells through druggable pathways. RNA profile of ceullar RNA and exosome of co-culture of breast caner cell line 1833 and stroma cell line MRC5.

2014-10-24 | E-GEOD-60997 | biostudies-arrayexpress

Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 2]

2014-10-24 | GSE60995 | GEO

Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 1]

2014-10-24 | GSE60994 | GEO

Analysis of exosome RNA from co-culture of cancer cell and stroma cell

Project description:How stroma communicates with cancer to influence treatment response is poorly understood. We show that stromal fibroblasts protect breast cancer (BrCa) against radiation and chemotherapy through an exosome-mediated anti-viral pathway and NOTCH3. Stroma increases RAB27B and transfers exosomes to BrCa. RNA within exosomes, comprised largely of non-coding transcripts and transposable elements, stimulates the pattern recognition receptor RIG-I through a 5’-triphosphate motif to activate STAT1. BrCa NOTCH3 is activated in parallel by stromal JAG1 and cooperates with STAT1 to enhance transcriptional responses of NOTCH target genes and to expand therapy resistant tumor-initiating cells. Computational modeling using primary human and mouse BrCa supports the interaction of anti-viral/NOTCH3 pathways in controlling NOTCH target genes and treatment resistance, particularly in basal subtype tumors. Gamma secretase inhibitors reverse stromal protection and abrogate radiation resistance in vivo. Thus, stroma orchestrates an intricate cross-talk with BrCa by utilizing exosomes to coax anti-viral signaling that expands therapy resistant cells through druggable pathways.

2014-10-24 | GSE60997 | GEO

Gene expression anlaysis of laser-capture microdissected tumor and stroma from triple negative breast cancer

Project description:LCM was perfomed on adjacent tumor and stromal cells to identify differentially expressed genes in triple negative breast cancer. To determine differences in tumor and adjacent stromal tissue, laser-capture microdissction was perfomed on 10 triple negative breast cancer specimans to isolate tumor and stromal cells for gene expression analysis. RNA was isolated from captured cells and hybridized to affymetrix gene expression microarrays.

2016-07-01 | E-GEOD-81838 | biostudies-arrayexpress

Expression data from a new lymphoid stromal population

Project description:Lymph node (LN) stromal cells provide survival signals and adhesive substrata to lymphocytes. During an immune response, B cell follicles enlarge, questioning how LN stromal cells manage these cellular demands. Herein, we used a murine fate mapping system to describe a new stromal cell type that resides in the T cell zone of resting LNs. We used microarrays to detail the global programme of gene expression characterizing this new population of lymphoid stromal cells. Mice lymph nodes were collected and digested before cell sorting and RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain homogeneous populations of lymphoid stromal cells in order to increase expression profiles.

2013-12-31 | E-GEOD-47906 | biostudies-arrayexpress

Expression data from exosomes

Project description:Bone marrow (BM) niches provide an optimal substrate for multiple myeloma (MM) cell lodgement and growth. Nevertheless, little is known about the putative mechanisms by which the BM microenvironment can lead to initiation or progression of oncogenesis in this disease. We have demonstrated that BM mesenchymal stromal cell-derived exosomes transfer their miRNA and protein content to clonal plasma cells, thus acting as synaptic vesicles responsible for molding the microenvironment surrounding multiple myeloma (MM) cells, leading to MM growth, dissemination and, therefore, disease progression. We used microarray to detail the changes in microRNA expression in MM-BM mesenchymal stromal cell (MSC)-derived exosomes, compared to normal- and monoclonal gammopathy of undetermined significance- BM-MSC-derived exosomes. Exosomes have been isolated from cell culture supernatant of BM-MSCs (MM=7; MGUS=2; Normal=4), and subsequently evaluated at ultrastructural level by using electron microscopy and immunogolf labeling. RNA was extracted; and miRNA profiling has been assessed by using TaqMan human miRNA profiling. Mean miRNA expression value has been used for miRNA RT-qPCR data normalization, as described (Mestdagh et al., 2009).

2013-07-24 | E-GEOD-39571 | biostudies-arrayexpress

Stromal and epithelial changes in breast cancer following endocrine treatment

Project description:Patients diagnosed with breast cancer were recruited to an important trial, the Tamoxifen Window Trial, in two series, series A during 1988-1989 and series B during 1989-1990. Some patients received tamoxifen for short windows. Clinical samples (biopsies) for this trial were collected before and after treatment. These biopsies were available as formalin-fixed paraffin-embedded (FFPE) tissue blocks. Responding patients and non-responding patients were determined by the change in the Ki67 scores. Responding patients were identified as those that had demonstrated a reduction in their Ki67 scores, and non-responding patients were identified as those in which Ki67 had not changed or had increased. The change in the percentage of Ki67 positive tumour cells was obtained by comparing the pre-treatment and post-treatment scores and calculating the difference in the scores. Laser capture microdissection (LCM) was utilised to microdissect the epithelial and stromal cells from the post-treatment breast cancer FFPE tissue sections of responding and non-responding patients. Samples obtained following LCM underwent RNA extraction and were subsequently used for gene expression profiling. Post-treatment samples from three responding patients (A29, B42, B61) and three non-responding patients (A15, A19, B59) were identified as suitable for this study and underwent LCM. Samples were analysed using Affymetrix GeneChipM-BM-. Human Exon 1.0 ST array. No technical replicates were performed. The stromal compartments collected from post-treatment samples of patients B59 and B61 failed to generate the appropriate yield of cDNA following two rounds of amplification and consequently were excluded from further analysis. Array hybridisation of samples were performed in 3 separate batches.

2014-07-07 | E-GEOD-58598 | biostudies-arrayexpress

Project description:Breast milk is a complex liquid that enriched in immunological components and affect the development of the infant immune system. Exosomes, the membranous vesicles of endocytic origin, are ubiquitously in various body fluids which can mediate intercellular communication. MicroRNAs (miRNAs), a well-defined group of non-coding small RNAs, in human breast milk are packaged inside exosomes. Here, we present the identification of miRNAs in human breast milk exosomes using deep sequencing technology. We found that the immune-related miRNAs are enriched in breast milk exosomes, and are resistant to the general harsh conditions. Four small RNA libraries in human breast milk exosomes from four healthy women (30 +/- 0.9 years old, primiparity) when the infant were aged at 60 days were sequenced.

2011-12-21 | E-GEOD-32253 | biostudies-arrayexpress

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