Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1145017 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30150316.fastq.gz | Fastqsanger.gz | |||
| SRR30150317.fastq.gz | Fastqsanger.gz | |||
| SRR30150318.fastq.gz | Fastqsanger.gz | |||
| SRR30150319.fastq.gz | Fastqsanger.gz | |||
| SRR30150320.fastq.gz | Fastqsanger.gz |
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Project description:Objective We have previously shown that expression of the CEACAM1 long isoform (CC1-L) in metastatic colorectal cancer (CRC) cells results in significant inhibition of liver metastasis via Chemokine (C-C motif) Ligand 2 (CCL2) and Signal Transducer and Activator of Transcription 3 (STAT3) signaling. Yet, despite recent advances in identifying molecules involved in the CC1-L inhibition of metastasis, much remains to be elucidated regarding the molecular mechanisms orchestrating this pathway. Design We performed an untargeted transcript profiling and a phosphokinase screen between CC1-L-expressing and non-expressing (CT) CRC cells. Identified targets were validated in vitro and in vivo for their involvement in signaling and invasion or metastasis. We validated our conclusions in CRC patient cohorts for time to metastasis development and long-term survival. Results Untargeted transcript profiling revealed high Decorin (Dcn) expression in CC1-L-expressing cells versus CT cells. Decorin was detected at the peri-endothelial layers of large blood vessels and in liver stellate cells. In metastatic lesions, it was expressed in pericyte-like cells covering capillary endothelium. Phosphokinase differential screening revealed reduced Ephrin type-A receptor 2 (EphA2) expression and activity in CC1-L- versus CT-expressing cells. Treatment of CT cells with recombinant Dcn led to decreased migration and invasion and decreased EphA2-mediated Erk and Akt signaling. CRC patients exhibiting high CC1 and DCN expression, in combination with low EPHA2 expression, benefit from longer 10-year survival than those with high EPHA2 expression. Conclusion CC1-L expression in poorly differentiated CRC inhibits liver metastasis through increased Decorin expression and EphA2-mediated signaling. Quadriplicate samples of each mouse colon cancer cell lines (control cells versus those expressing either short or long isoform of CEACAM1) have been used for RNA extraction
2015-09-19 | E-GEOD-73208 | biostudies-arrayexpress
Project description:Objective We have previously shown that expression of the CEACAM1 long isoform (CC1-L) in metastatic colorectal cancer (CRC) cells results in significant inhibition of liver metastasis via Chemokine (C-C motif) Ligand 2 (CCL2) and Signal Transducer and Activator of Transcription 3 (STAT3) signaling. Yet, despite recent advances in identifying molecules involved in the CC1-L inhibition of metastasis, much remains to be elucidated regarding the molecular mechanisms orchestrating this pathway. Design We performed an untargeted transcript profiling and a phosphokinase screen between CC1-L-expressing and non-expressing (CT) CRC cells. Identified targets were validated in vitro and in vivo for their involvement in signaling and invasion or metastasis. We validated our conclusions in CRC patient cohorts for time to metastasis development and long-term survival. Results Untargeted transcript profiling revealed high Decorin (Dcn) expression in CC1-L-expressing cells versus CT cells. Decorin was detected at the peri-endothelial layers of large blood vessels and in liver stellate cells. In metastatic lesions, it was expressed in pericyte-like cells covering capillary endothelium. Phosphokinase differential screening revealed reduced Ephrin type-A receptor 2 (EphA2) expression and activity in CC1-L- versus CT-expressing cells. Treatment of CT cells with recombinant Dcn led to decreased migration and invasion and decreased EphA2-mediated Erk and Akt signaling. CRC patients exhibiting high CC1 and DCN expression, in combination with low EPHA2 expression, benefit from longer 10-year survival than those with high EPHA2 expression. Conclusion CC1-L expression in poorly differentiated CRC inhibits liver metastasis through increased Decorin expression and EphA2-mediated signaling.
2015-09-19 | GSE73208 | GEO
Project description:Limbal stem cells including epithelial and stromal/Mesenchymal stem cells that contribute to sustained corneal homeostasis, maintain their ability to act as self-renewal progenitor cells by virtue of their limbal niche and intercellular communication. Extracellular vehicles (EVs), including exosomes (Exos), are important paracrine mediators through their cargo transfer for intercellular communication in various stem cell niches. Previously we have shown the differential cargos and regulatory roles of limbal stromal cell (LSC)-derived Exos, in limbal epithelial cells (LEC) in normal (N) and diabetic (DM) limbal niche. In the present study, to have a comprehensive knowledge of reciprocal LEC-LSC crosstalk, we investigated the proteomics and miRNA profile of exosomes derived from LEC and their regulatory roles in LSC in N and DM limbus. Our study showed wound healing and proliferation rates in primary N-LSC were significantly enhanced upon treatment by normal LEC-derived Exos (N-Exos), but not by diabetic Exos (DM-Exos). Further, N-Exos treated LSC showed downregulation of keratocyte markers, ALDH3A1 and lumican, but not keratocan, and upregulation of MSC markers, CD105, CD90, and CD73 compared to the DM-Exos treated LSC. Using next generation sequencing (NGS) and proteomics analysis, we revealed some miRNAs and proteins in the Exos that affect the cellular crosstalk and the function of the cornea. We also documented differences in DM vs. normal LEC-derived Exo’s cargos. Overall, DM-Exos have less effect on LSC proliferation, wound healing, and stem cell maintenance than N-Exos, likely by transferring their cargo proteins and/or regulatory miRNAs targeting cell cycle, ERK/MAPK, TGF-β, EMT, PI3K-Akt-mTOR signaling molecules. This suggests that the small RNA and protein cargo differences in DM vs. N LEC-derived Exos could contribute to the disease state. Our study revealed a complex contribution of Exos to health and diabetic state of corneal homeostasis and suggests the potential of EV therapeutics for diabetic cornea regenerative medicine
2023-10-23 | PXD040918 | Pride
Project description:Epithelial and stromal/mesenchymal limbal stem cells contribute to corneal homeostasis and cell renewal. Extracellular vesicles (EVs), including exosomes (Exos), can be paracrine mediators of intercellular communication. Previously, we described cargos and regulatory roles of limbal stromal cell (LSC)-derived Exos in non-diabetic (N) and diabetic (DM) limbal epithelial cells (LEC). Presently, we quantify the miRNA and proteome profiles of human LEC-derived Exos and their regulatory roles in N- and DM-LSC. We revealed some miRNA and protein differences in DM vs. N-LEC-derived Exos' cargos including proteins involved in Exo biogenesis and packaging that may affect Exo production and ultimately cellular crosstalk and corneal function. Treatment by N-Exos, but not by DM-Exos enhanced wound healing in cultured N-LSC and increased proliferation rate in N and DM LSCs vs. corresponding untreated (control) cells. N-Exos treated LSC reduced keratocyte markers ALDH3A1 and lumican, and increased MSC markers CD73, CD90 and CD105 vs. control LSC. These being opposite to the changes quantified in wounded LSCs. Overall, N-LEC Exos have a more pronounced effect on LSC wound healing, proliferation, and stem cell marker expression than DM-LEC Exos. This suggests that regulatory miRNA and protein cargo differences in DM- vs. N-LEC-derived Exos could contribute to the disease state.
2023-09-29 | GSE243345 | GEO
Project description:Intervention type:DRUG. Intervention1:Huaier, Dose form:GRANULES, Route of administration:ORAL, intended dose regimen:20 to 60/day by either bulk or split for 3 months to extended term if necessary. Control intervention1:None.
Primary outcome(s): For mRNA libraries, focus on mRNA studies. Data analysis includes sequencing data processing and basic sequencing data quality control, prediction of new transcripts, differential expression analysis of genes. Gene Ontology (GO) and the KEGG pathway database are used for annotation and enrichment analysis of up-regulated genes and down-regulated genes.
For small RNA libraries, data analysis includes sequencing data process and sequencing data process QC, small RNA distribution across the genome, rRNA, tRNA, alignment with snRNA and snoRNA, construction of known miRNA expression pattern, prediction New miRNA and Study of their secondary structure Based on the expression pattern of miRNA, we perform not only GO / KEGG annotation and enrichment, but also different expression analysis.. Timepoint:RNA sequencing of 240 blood samples of 80 cases and its analysis, scheduled from June 30, 2022..
| 2612481 | ecrin-mdr-crc
Project description:We detected and compared the miRNAs contained in Y-PRP-exos or O-PRP-exos. The results showed that most miRNAs (38) can be identified in both Y-PRP-exos and O-PRP-exos. In addition, hsa-let-7f-5p, hsa-miR-16-5p and hsa-miR-126-3p were top 3 enriched miRNAs in PRP-exos of all donors. These results indicated the heterogeneity of miRNAs in PRP-exos was small, regardless of age. However, the abundance of miRNAs in Y-PRP-exos and O-PRP-exos was quite different, especially in high-ranking miRNAs. The expression of hsa-miR-16-5p and has-let-7f-5p in O-PRP-exos in two old donors was only approximately 1/4-1/2 of that in Y-PRP-exos in two young donors
2023-11-30 | GSE234781 | GEO
Project description:Posterior amorphous corneal dystrophy (PACD) is a rare, autosomal dominant disorder affecting the cornea and iris. After next-generation sequencing of the family in which linkage analysis identified a chromosomal locus for PACD on 12q21.33 failed to yield a pathogenic mutation, array-based copy number analysis and qPCR detected a deletion on 12q21.33 containing four genes encoding small leucine-rich proteoglycans (SLRPs): KERA, LUM, DCN, and EPYC. Two other families with PACD also demonstrated deletion of these SLRPs, which together with murine models of KERA, LUM, and DCN deficiency provide convincing evidence that PACD is caused by haploinsufficiency of these SLRPs.
2014-06-04 | GSE50573 | GEO
Project description:Primary cardiac myocytes isolated from neonatal Wistar rats were cultured and simulated ischemia/reperfusion injury were conducted on them in the presence or absence of decorin. Decorin is a small leucin-rich proteoglycan, which has a cardiocytoprotective effect. The underlaying mechanism of this cardiocytoprotective phenomenon is unknown, therefore our aim was to investigate the changes in the mRNA expression between the decorin (3nM) treated and vehicle-treated control cells.
2020-12-31 | E-MTAB-9325 | biostudies-arrayexpress
Project description:Purpose: Next-Generation Sequencing (NGS) RNA was subjected to analysis genome-wide expression. The goals of this study are to identify differentially expressed genes in CXCR4 knockout macrophages compared to CXCR4-expressed macrophages. Methods: Total RNA of macrophage transfected with CXCR4 siRNA (MΦsiCXCR4) or siRNA negative control (MΦsiNC), then, stimulated with 100ng/ml lipopolysaccharide (LPS) for 12 hours. Preparation of library and sequencing of transcriptome was performed by Illumina NovaSeq 6000. Results: A large number of differentially expressed genes were screened by high-throughput sequencing at the genome-wide level using RNA-Seq technology. Loss of CXCR4 in bone-marrow-derived macrophages results in attenuated pro-inflammatory cytokine and decorin production under LPS stimulation compared to control macrophages. Conclusions: Our study reveals that CXCR4 orchestrated the pro-inflammatory cytokine and decorin production in macrophages.
2023-08-06 | GSE182050 | GEO