Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tracing the evolution of single-cell 3D genomes in Kras-driven cancers

ABSTRACT: Tracing the evolution of single-cell 3D genomes in Kras-driven cancers

PROVIDER: PRJNA1151718 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30357931_1.fastq.gz	Fastqsanger.gz
	SRR30357931_2.fastq.gz	Fastqsanger.gz
	SRR30357932_1.fastq.gz	Fastqsanger.gz
	SRR30357932_2.fastq.gz	Fastqsanger.gz
	SRR30357933_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Tracing the evolution of single-cell 3D genomes in Kras-driven cancers

Project description:Although three-dimensional (3D) genome structures are altered in cancer cells, little is known about how these changes evolve and diversify during cancer progression. Leveraging genome-wide chromatin tracing to visualize 3D genome folding directly in tissues, we generated 3D genome cancer atlases of oncogenic Kras-driven murine lung and pancreatic adenocarcinoma. Our data reveal stereotypical, non-monotonic, and stage-specific alterations in 3D genome folding compaction, heterogeneity, and compartmentalization as cancers progress from normal to preinvasive and ultimately to invasive tumors, discovering a potential structural bottleneck in early tumor progression. Remarkably, 3D genome architectures distinguish morphologic cancer states in single cells, despite considerable cell-to-cell heterogeneity. Gene-level analyses of evolutionary changes in 3D genome compartmentalization not only showed that compartment-associated genes are more homogeneously regulated but also elucidated prognostic and dependency genes in lung adenocarcinoma and a previously unappreciated role for polycomb-group protein Rnf2 in 3D genome regulation. Our results demonstrate the utility of mapping the single-cell cancer 3D genome in tissues and illuminate its potential to identify new diagnostic, prognostic, and therapeutic biomarkers in cancer.

2025-05-02 | GSE295857 | GEO

Tracing the evolution of single-cell 3D genomes in Kras-driven cancers

2025-05-24 | GSE275588 | GEO

Tracing the evolution of single-cell 3D genomes in Kras-driven cancers [snRNA-seq]

2025-05-24 | GSE295452 | GEO

Tracing the evolution of single-cell 3D genomes in Kras-driven cancers

Project description:Tracing the evolution of single-cell 3D genomes in Kras-driven cancers

| PRJNA1256505 | ENA

Tracing the evolution of single-cell 3D genomes in Kras-driven cancers [snRNA-seq]

Project description:Tracing the evolution of single-cell 3D genomes in Kras-driven cancers [snRNA-seq]

| PRJNA1254700 | ENA

Tracing the lineage of replicative RNAs in the process of KRAS (S17N) evolution

Project description:A dominant-negative gene therapy approach has been proposed and tested on proto-oncogene KRAS, wherein the oncogenic activity (and cell proliferation) of KRAS can be suppressed by introducing a dominant-negative KRAS allele (S17N). We employed REPLACE to conduct continuous evolution on KRAS (S17N) and examined its potential pathways for conferring resistance in this gene therapy methodology.To explore the accumulation of mutations in various RNAs during the KRAS (S17N) evolution experiment, we established a barcoded library and conducted lineage tracing of replicative RNAs carrying KRAS (S17N) throughout the evolution process.

2024-09-30 | GSE271874 | GEO

Protein-RNA interaction dynamics downstream of KRAS activation reveals key regulators of oncogenic KRAS driven cancers.

Project description:Oncogenic KRAS mutations rewires cellular signaling, leading to significant alterations in gene expression. RNA-binding proteins (RBPs) play a pivotal role in gene expression regulation by post-transcriptionally controlling various aspects of RNA metabolism. It becomes clear that interactions between RBPs and RNA are frequently dysregulated in numerous cancers. However, how the oncogenic KRAS mutations reshape the post-transcriptional regulatory network mediated by RBPs remain poorly understood. In this study, we have systematically dissected oncogenic KRAS driven alternation of RNA-RBP networks. We identified several cancer-associated RBPs with either increased or decreased RNA binding upon oncogenic KRAS, including PDCD11, which is essential for the viability of KRAS mutant cancers, and ELAVL2, which regulates SNAIL and affects cell migration in KRAS mutant lung cancers. Our study serves as a crucial resource for elucidating RBP regulatory networks in KRAS mutant cancers and may provide new avenues for therapeutic strategies targeting KRAS mutant malignancies.

2025-05-07 | PXD053310 | Pride

A proteomic and phosphoproteomic landscape of KRAS mutant cancers identifies combination therapies

Project description:KRAS mutant cancers, which feature the activation of multiple phosphorylation signaling pathways, remain a major challenge for cancer therapy. This study provides a landscape of the proteomics and phosphoproteomics of KRAS mutant cancers by analyzing different KRAS mutant human cancer cell lines across different tissues types. By integrating multi-omics analysis, we identify different robust subsets, which recapitulate the histological, pathological and prognostic features of human cancers.

2021-06-23 | PXD026892 |

BI-3406, a potent and selective SOS1::KRAS interaction inhibitor, is effective in KRAS-driven cancers through combined MEK inhibition

Project description:KRAS is the most frequently mutated driver of pancreatic, colorectal, and non-small cell lung cancers. Direct KRAS blockade has proven challenging and inhibition of a key downstream effector pathway, the RAF-MEK-ERK cascade, has shown limited success due to activation of feedback networks that keep the pathway in check. We hypothesized that inhibiting SOS1, a KRAS activator and important feedback node, represents an effective approach to treat KRAS-driven cancers. We report the discovery of a highly potent, selective and orally bioavailable small-molecule SOS1 inhibitor, BI-3406, that binds to the catalytic domain of SOS1 thereby preventing the interaction with KRAS. BI-3406 reduces formation of GTP-loaded RAS and limits cellular proliferation of a broad range of KRAS-driven cancers. Importantly, BI-3406 attenuates feedback reactivation induced by MEK inhibitors and thereby enhances sensitivity of KRAS-dependent cancers to MEK inhibition. Combined SOS1 and MEK inhibition represents a novel and effective therapeutic concept to address KRAS-driven tumors.

2020-08-20 | GSE128385 | GEO

Tracing the lineage of replicative RNAs in the process of KRAS (S17N) evolution

Project description:Tracing the lineage of replicative RNAs in the process of KRAS (S17N) evolution

| PRJNA1133787 | ENA