Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-43306
PROVIDER: PRJNA185391 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR645769_1.fastq.gz | Fastqsanger.gz | |||
| SRR645769_2.fastq.gz | Fastqsanger.gz | |||
| SRR645770_1.fastq.gz | Fastqsanger.gz | |||
| SRR645770_2.fastq.gz | Fastqsanger.gz | |||
| SRR645771_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:CXCL12 and IGF1 are key secreting molecules produced by cancer-associated fibroblasts in breast cancer. These factors promote the survival of disseminated cancer cells in the bone marrow. To assess the combined responses elicited by CXCL12 and IGF1, we examined the translating transcriptome of cancer cells in response to these two factors by Translating Ribosome Affinity Purification (TRAP)-RNAseq. MDA-MB-231 cells were engineered to express an EGFP-tagged version of ribosomal protein L10a. This allows the retrieval of polysome-associated mRNA by anti-GFP pull down (TRAP) and profiling the translating transcriptome by RNAseq. EGFP-L10a+ cancer cells were serum starved (0.2% serum) for 24 hours, and then treated with CXCL12 (30ng/mL) + IGF1 (10ng/mL) or CXCL12 (300ng/mL) + IGF1 (100ng/mL) for 6hrs. Two biological replicates were profiled for each condition.
2013-11-01 | E-GEOD-43296 | biostudies-arrayexpress
Project description:CXCL12 and IGF1 are key secreting molecules produced by cancer-associated fibroblasts in breast cancer. These factors promote the survival of disseminated cancer cells in the bone marrow. To assess the combined responses elicited by CXCL12 and IGF1, we examined the translating transcriptome of cancer cells in response to these two factors by Translating Ribosome Affinity Purification (TRAP)-RNAseq.
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Project description:CXCL12 and IGF1 confer on cancer cells survival advantage. Src potentiates cancer cells' reponse to CXCL12 and IGF1 by strengthening AKT activation. Long-term incubation of CXCL12 and IGF1 select for cancer cells with enhanced Src activity and bone metastasis potential. MDA-MB-231 cells were incubated for three weeks in growth medium of reduced serum concentration (0.2%) with or without CXCL12 (30 ng/ml) and IGF1 (10 ng/ml). Cell populations survive under these condidtions are expanded by regular growth medium with 10% serum. Two biological replicates were profiled for each condition.
2012-12-10 | E-GEOD-39102 | biostudies-arrayexpress
Project description:CXCL12 and IGF1 confer on cancer cells survival advantage. Src potentiates cancer cells' reponse to CXCL12 and IGF1 by strengthening AKT activation. Long-term incubation of CXCL12 and IGF1 select for cancer cells with enhanced Src activity and bone metastasis potential.
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Project description:How organ-specific metastatic traits accumulate in primary tumors remains unknown. We identified a role of the primary tumor stroma in selecting breast cancer cells that are primed for metastasis in the bone. A fibroblast-rich stroma in breast tumors creates a microenvironment that is similar to that of bone metastases in its abundance of the cytokines CXCL12 and IGF1. Heterogeneous breast cancer cell populations growing in such mesenchymal environment evolve towards a preponderance of clones that thrive on CXCL12 and IGF1. Fibroblast-driven selection of bone metastatic clones in mammary tumors is suppressed by CXCL12 and IGF1 receptor inhibition. Thus, a fibroblast-rich stroma in breast tumors can pre-select bone metastatic seeds, promoting the evolution of metastatic traits and the interplay between a primary tumor and its distant metastases. Affymetrix U133 Plus2 arrays were hybridized according to the manufacturer's procedure using RNA extracted from 47 primary breast tumors. Specific gene sets were evaluated in this cohort.
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Project description:How organ-specific metastatic traits accumulate in primary tumors remains unknown. We identified a role of the primary tumor stroma in selecting breast cancer cells that are primed for metastasis in the bone. A fibroblast-rich stroma in breast tumors creates a microenvironment that is similar to that of bone metastases in its abundance of the cytokines CXCL12 and IGF1. Heterogeneous breast cancer cell populations growing in such mesenchymal environment evolve towards a preponderance of clones that thrive on CXCL12 and IGF1. Fibroblast-driven selection of bone metastatic clones in mammary tumors is suppressed by CXCL12 and IGF1 receptor inhibition. Thus, a fibroblast-rich stroma in breast tumors can pre-select bone metastatic seeds, promoting the evolution of metastatic traits and the interplay between a primary tumor and its distant metastases.
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Project description:CXCL12 and IGF1 select for cancer cell populations with enhanced bone metastasis ability
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Project description:Translation is the process by which genetic information from mRNA is decoded to produce proteins. Since mRNA levels alone do not predict protein amounts accurately, understanding translational control is essential. Ribosome profiling revealed that translation initiation is the main rate-limiting step, with rates varying up to 100-fold across mRNAs, while elongation rates vary less (~20-fold). Furthermore, only a small fraction of the variation in translation rates is explained by known determinants, indicating that much remains to be understood in the prediction of protein outputs of individual mRNAs. Current machine learning models would benefit from more data on endogenous mRNAs. To address this, here we report steady-state and dynamic multi-omics data from human liver cancer cell lines, specifically i) ribosome profiling of unperturbed cells and following translation initiation block to trace elongation (run-off ribosome profiling), ii) protein synthesis rates estimated by pulsed stable isotope labeled amino acids in cell culture (pSILAC), and iii) mean ribosome load on individual mRNAs determined by mRNA sequencing of polysome fractions (polysome profiling). Predicting protein output from mRNAs is crucial for applications like protein expression engineering or mRNA vaccine designing.
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