Ontology highlight
ABSTRACT:
PROVIDER: PRJNA950113 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24010100_1.fastq.gz | Fastqsanger.gz | |||
| SRR24010100_2.fastq.gz | Fastqsanger.gz | |||
| SRR24010101_1.fastq.gz | Fastqsanger.gz | |||
| SRR24010101_2.fastq.gz | Fastqsanger.gz | |||
| SRR24010102_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 34 |
Similar Datasets
Project description:We performed RNA-sequencing to investigate the gene expression profiles of colorectal cancer patient-derived organoids (PDO) and PDO-initiated spontaenous metastases mouse models
2022-12-01 | GSE213896 | GEO
Project description:Zonation of the Vitis vinifera microbiome in Vino Nobile di Montepulciano PDO production area
| PRJEB75007 | ENA
Project description:Primary objectives: percentuale di pazienti che saranno sottoposti a resezione completa
Primary endpoints: Lo Studio si propone di aumentare la percentuale di resecabilita’ di pazienti con metastasi epatiche da carcinoma del colon retto.
| 2517634 | ecrin-mdr-crc
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare the epigenomes of different patient-derived models of colorectal cancer (PDO, PDX and PDOX) to the original patient tumor. Methods: The Omni-ATAC protocol was utilized for ATAC library preparations. The nulcei were extracted from samples (PT, PDO, PDX and PDOX). For each sample set, three biological replicates were included. The libraries were sequenced using Illumina HiSeq 4000 PE 150bp. Results: Using an optimized data analysis workflow, we achieved high quality ATAC-seq library. Data were mapped to hg19 with over 90% mapping rate, and relative low mitochondria fraction (<30%). We used Diffbind to assess the chromatin accessibility enrichment in each model with a strict threshold of p <0.05 and |logFC|>1. Conclusions: Our study represents the first detailed analysis of CRC PDMC epigenome. CRC cells from all three models share chromatin alterations when compared to PT cells, representing a PT-PDMC epigenetic axis. Chromatin alterations in CRC cells are more similar betweeen PDOX and PDX than between PDOX and PDO, indicating that the growth environment of the model exerts strong influence on chraomtin adaptation in tumor cells.
2024-03-01 | GSE184482 | GEO
Project description:To investigate degradation genes in the 3HP degradation pathway, transcriptome sequencing was performed under culture conditions with and without 3HP as the carbon source. Overall, in the presence of 3HP as a sole carbon source, 384 genes were upregulated while 210 downregulated. Among them, we identified two 3HP degradation genes, GME_RS01260 encoding choline dehydrogenase (RefSeq. Accession: WP_009721523) and GME_RS01255 encoding CoA-acylating methylmalonate-semialdehyde dehydrogenase (RefSeq. Accession WP_009721522). Subsequently, transcriptome sequencing was performed under the culture condition with or without addition of PDO as a carbon source. Overall, 292 genes were upregulated while 285 downregulated with the addition of PDO. Among them, we identified an alcohol dehydrogenases AdhP (RefSeq. Accession: WP_039868491.1).
2021-01-01 | GSE159233 | GEO
Project description:Natural killer (NK) cells represent a promising strategy for cellular cancer immunotherapy, but it remains unclear which patients benefit by such therapies. Using co-cultures of primary human allogenic NK cells and patient-derived colon cancer organoids (PDOs), we could stratify PDOs into NK cell “highly susceptible” and “rather resistant” groups reflected by differential expression of NKG2D-ligands, MHC class I and CEACAM. RNA-seq unveiled that hypoxia- and TGF-β-related gene signatures were induced in NK cells after PDO co-culture. Deletion of hypoxia inducible factor (HIF)-2a in primary NK cells or blocking of TGF-β-R1 empowered NK cell-mediated PDO killing. We further demonstrate that upon PDO killing, NK cells adopted an activation/inflammationhigh, cytotoxicitylow, tissue-residencyhigh program as evidenced by CXCR6 and CD49a expression coinciding with a “hot” cytokine/chemokine-rich microenvironment. Since PDO-exposed NK cells largely resemble features of NK cells from CRC patient tissues, our NK cell/PDO platform could be highly relevant for the optimization of NK cell products for personalized medicine.
2025-12-17 | GSE292020 | GEO
Project description:The cholera disease bacterium V. cholerae, can adopt planktonic or biofilm lifestyles depending on the intracellular concentration of the second messenger cyclic diguanylic acid (c-di-GMP). Biofilm formation protects Vibrios from stressful conditions and facilitates disease transmission by enhancing infectivity. The histone-like nucleoid structuring protein (H-NS) is a global regulator of genes associated with pathogenicity and responses to environmental stresses. H-NS represses the transcription of genes vpsT, vpsA and vpsL, which are required for the biosynthesis of the biofilm exopolysacchide matrix. Here we demonstrate that the c-di-GMP-binding protein VpsT disrupts H-NS nucleoprotein complexes at the vpsA and vpsL promoters and that this effect is enhanced by c-di-GMP. We used ChIP coupled with Next Generation Sequencing (ChIP-Seq) and transcriptome analysis (RNA-Seq) to identify additional loci repressed by H-NS affecting biofilm formation. This study showed that H-NS directly represses the transcription of genes encoding proteins present in the biofilm matrix such as the rbmA-F cluster, hemolysin and chitinase. Similar to vpsA and vpsL, the promoter region of vpsU, rbmA and rbmF exhibited overlapping H-NS and VpsT binding motifs. Deletion of vpsT increased H-NS occupancy at the vpsU, vpsA, vpsL, rbmA and rbmF promoters. Conversely, artificially increasing the c-di-GMP pool diminished H-NS occupancy at the above promoters. Deletion of vpsT did not affect H-NS occupancy at its own promoter. However, deletion of genes encoding the regulators AphA and VpsR significantly increased H-NS occupancy at the vpsT promoter. In sum, our study shows that c-di-GMP enhances biofilm formation by acting through VpsT to activate an H-NS anti-repression cascade. The Binding profile of V. cholerae H-NS to the genome was determined by ChIP followed by Next Generation Sequencing (ChIP-Seq) using the Illumina HiSeq2000 platform. V. cholerae C7258 cells expressing H-NS-FLAG fusion protein from the hns transcription and translation signals were collected from LB cultures grown to mid-exponential phase (OD600 0.5). An anti-FLAG Immunoprecipitation (IP) and an Input samples were used for the analysis.
2015-05-13 | E-GEOD-64249 | biostudies-arrayexpress