Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260054 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1562814_1.fastq.gz | Fastqsanger.gz | |||
| SRR1562814_2.fastq.gz | Fastqsanger.gz | |||
| SRR1562815_1.fastq.gz | Fastqsanger.gz | |||
| SRR1562815_2.fastq.gz | Fastqsanger.gz | |||
| SRR1562816_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 2]
| PRJNA260055 | ENA
Project description:Exosome Transfer from Stromal to Breast Cancer Cells Regulates Therapy Resistance Pathways [set 1]
| PRJNA260056 | ENA
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
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
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
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-60994 | biostudies-arrayexpress
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.
2014-10-24 | GSE60995 | GEO
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.
2014-10-24 | GSE60994 | GEO
Project description:Most cancer deaths result from progression of therapy resistant disease, yet our understanding of this phenotype is limited. Cancer therapies generate stress signals that act upon mitochondria to initiate apoptosis. Mitochondria isolated from neuroblastoma cells were exposed to tBid or Bim, death effectors activated by therapeutic stress. Multidrug resistant tumor cells obtained from children at relapse had markedly attenuated Bak and Bax oligomerization and cytochrome c release (surrogates for apoptotic commitment) in comparison with patient-matched tumor cells obtained at diagnosis. Electron microscopy identified reduced endoplasmic reticulum-mitochondria contacts (ERMCs) in therapy resistant cells, and genetically or biochemically reducing ERMCs in therapy sensitive tumors phenocopied resistance. ERMCs serve as platforms to transfer Ca2+ and bioactive lipids to mitochondria. Reduced Ca2+ transfer was found in some but not all resistant cells, and inhibiting transfer did not attenuate apoptotic signaling. In contrast, reduced ceramide synthesis and transfer was common to resistant cells and its inhibition induced stress resistance. We identify ERMCs as physiologic regulators of apoptosis via ceramide transfer and uncover a previously unrecognized mechanism for cancer multidrug resistance.
2021-11-18 | ST002054 | MetabolomicsWorkbench
Project description:This study provides a novel mechanism that RAS activation of breast cancer cells induces osteolytic bone metastasis by stimulating the exosome-mediated transfer of osteoclastogenic miRNAs including miR-494-3p to bone cells
2023-07-12 | GSE235802 | GEO