Gene expression analysis of tumors of TN and R clonal pairs in vivo
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA578861 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10322859.fastq.gz | Fastqsanger.gz | |||
| SRR10322860.fastq.gz | Fastqsanger.gz | |||
| SRR10322861.fastq.gz | Fastqsanger.gz | |||
| SRR10322862.fastq.gz | Fastqsanger.gz | |||
| SRR10322863.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 30 |
Similar Datasets
Project description:We previously had generated clonal mouse melanoma cell lines, where each clone was isolated in a RAFi/MEKi-resistant ( R ) or treatment-naïve ( TN ) state using the method CaTCH (clones: 2646TN, 2646R, 14559TN, 14559R, 13TN). We assessed the response to targeted therapy of these clones in in vivo experiments using RAFi/MEKi-treatments. Herey, we saw that, compared to the other treatment-naïve clones, 2646TN exhibited a strongly reduced response to targeted therapy. 2646TN displayed fast growth on drug after only five days, indicating an increased persistence and fast adaption to the treatment, while all other TN clones responded to the treatments and showed tumor regression for weeks before relapsing. To uncover intrinsic programs that might underlie th minimal response of 2646TN, we examined the transcriptome of untreated and short-term treated tumors comprising 2646TN, 2646R, 14559TN, 14559R, or 13TN clones . These clonal cell lines were injected subcutaneously into C57BL/6 mice and tumors were harvested either at tumor engraftment (untreated) or after 3 days of RAFi/MEKi treatment. Lviving cancer cells were sorted from the tumors by FACS and the markers CD45- and the cell line specific marker GFP+. Libraries were prepared using the Lexogen Quantseq 3' mRNA seq kit and sqeuencing was performed on an Illumina HiSeqV4 sequencer (single-read 50 read mode).
2020-07-20 | GSE139236 | GEO
Project description:Acinetobacter baumannii in vivo Tn-seq
| PRJEB83056 | ENA
Project description:Tn antigen (Tn), a single N-acetylgalactosamine (GalNAc) monosaccharide attached to protein Ser and Thr residues, is found on most solid tumors yet rarely detected in adult tissues: featuring it one of the most distinctive signatures of cancers. Although it is prevalent in cancers, Tn-glycosylation sites are not entirely clear owing to the lack of suitable technology. Knowing the Tn-glycosylation sites will spur the development of the new vaccines, diagnostics, and therapeutics of cancers. Here, we report a novel technology named EXoO-Tn for large-scale mapping of Tn-glycosylation sites. EXoO-Tn utilizes glycosyltransferase C1GalT1 and isotopically-labeled UDP-Gal(13C6) to tag and convert Tn to Gal(13C6)-Tn. This exquisite Gal(13C6)-Tn structure is recognized by a human-gut-bacterial enzyme, called OpeRATOR, that specifically cleaves N-termini of the Gal(13C6)-Tn-occupied Ser and Thr residues to yield site-containing glycopeptides. The enzymes C1GalT1 and OpeRATOR could be used concurrently in one-pot. The effectiveness of EXoO-Tn was evaluated by analyzing Jurkat cells, where 947 Tn-glycosylation sites from 480 glycoproteins were mapped. Bioinformatic analysis of the identified site-specific Tn-glycoproteins revealed conserved motif, cellular localization, relative position in proteins, and mapped site-specific Tn-glycoproteome in different studies. Given the significance of Tn in cancers, EXoO-Tn is anticipated to have broad utilities in clinical study of cancers.
2022-02-15 | PXD014390 | Pride
Project description:Clonal relatedness in tumour pairs of breast cancer patients
| PRJNA429337 | ENA
Project description:Aberrant O-glycosylation and accumulation of the Tn antigen are associated with aggressive phenotypes in triple-negative breast cancer (TNBC). To investigate the transcriptomic consequences of Tn antigen expression, we analyzed gene expression profiles of murine 4T1 breast cancer cells carrying CRISPR/Cas9-mediated silencing of the Cosmc gene (Tn+) compared with parental wild-type 4T1 cells (WT). Total RNA was extracted from 4T1 cells-bearing tumors from mice (Tn and WT)s and subjected to RNA sequencing using Illumina NovaSeq X technology.
2026-06-10 | GSE332663 | GEO
Project description:To investigate the systemic impact of Tn+ tumor phenotypes, we conducted an analysis of circulating miRNAs in the serum of mice bearing Tn+- 4T1 tumors. The 4T1/Tn+ cell line was generated via CRISPR/Cas9 targeting of Cosmc, and tumors were established orthotopically in BALB/c mice. Tumor-bearing animals were monitored for primary growth and micrometastatic dissemination to the lungs, followed by serum collection at endpoint. Serum samples were pooled according to tumor Tn status (Tn+ or Tn–) for total RNA extraction, including small RNAs. Using the NanoString nCounter Mouse v1.5 miRNA assay, we profiled miRNA expression in three serum pools (two Tn+, one Tn–), followed by normalization and quality control via the nCounter Advanced Analysis Software. Expression values were normalized using geometric means of internal positive and negative controls, and only stable miRNA regions (CV < 15%) were retained for downstream analysis.
2026-06-23 | GSE302365 | GEO
Project description:Clonal Analyses of Refractory Testicular Germ Cell Tumors
| PRJNA508792 | ENA
Project description:Light dependent gene expression in D. shibae wildtype compared to the gene expression in the transposonmutants D. shibae Dshi_1135::Tn, D. shibae ppaA::Tn and D. shibae ppsR::Tn. Dinoroseobacter shibae DFL12T (DSM 16493T) and the transposonmutants D. shibae Dshi_1135::Tn, D. shibae ppaA::Tn and D. shibae ppsR::Tn were grown in artificial saltwater minimal medium (SWM) in baffled flasks shaking at 180 rpm and 30 °C and incubation was performed under light, dark and bluelight conditions. D. shibae wild type and mutant strain were grown under aerobic conditions up to the mid exponential growth phase (OD578 nM 0.5).
2023-10-01 | GSE244289 | GEO
Project description:We used DNA content-based flow cytometry to distinguish and isolate nuclei of clonal tumor populations from primary and metastatic refractory testicular germ cell tumors (TGCTs) tissues. We then interrogated each sorted tumor populationwith whole genome aCGH and next generation sequencing (NGS). we have explored the clonal basis of refractory TGCT by investigating distinct tumor populations that were present in each tumor. Notably this included resected primary tissues and treatment refractory metastases that arose after high dose chemotherapy. These results provide new knowledge regarding the role of clonal selection and selected genomic lesions in the resistance to chemotherapy in TGCT within this exceptional cohort.
2019-02-26 | GSE123464 | GEO
Project description:Maintenance of T cell naïve (Tn) state and restricting effector T cell differentiation upon basal level stimulations would be critical for immune homeostasis and prevention of autoimmunity. To understand how Tn state is regulated by nutrient cues in a cell-intrinsic manner, here we perform an in vivo CRISPR screening to identify required solute carrier (SLC) proteins that transport metabolites and ions into T cells. Among SLC proteins revealed by this experiment, vitamin C transporter Slc23a2 appears to play a role. Conditional ablation of Slc23a2 in T cells by genetic approaches reduces intracellular vitamin C levels by approximately 80%, accompanied by spontaneous activation and differentiation of Tn cells, autoantibody production, and autoimmune pathology in select organs. Slc23a2-deficient Tn cells exhibit profound DNA hypermethylation, dysregulation of genes controlling signaling transduction and transcription, and enhanced differentiation of helper T cells upon stimulation. These results define a broad regulatory space of vitamin C as a cofactor of Tet enzymes in controlling active DNA demethylation. In agreement, conditional deletion of Tet genes impairs Tn state and increases helper T cell differentiation. Thus, our study reveals a cell-intrinsic mechanism by which micronutrient vitamin C via Slc23a2 maintains Tn state and self-tolerance by promoting Tet-mediated DNA demethylation.
2026-05-08 | GSE261456 | GEO