Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE140497 | GEO | 2020/02/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice [Cut&Run]

Project description:In most cancers, only a few genes are mutated at high frequencies, while the vast majority are mutated at low frequencies. The functions of these recurrent but infrequent ‘long-tail’ mutations remain largely elusive. Here, we develop in vivo CRISPR screens to assess the transforming potential of 484 long-tail genes in human Head and Neck Squamous Cell 5 Carcinoma (HNSCC).

2020-02-04 | GSE140496 | GEO

In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice [RNA-seq]

2020-02-04 | GSE140495 | GEO

In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice

Project description:In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice

| PRJNA589893 | ENA

In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice [RNA-seq]

Project description:In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice [RNA-seq]

| PRJNA589896 | ENA

In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice [Cut&Run]

Project description:In vivo CRISPR screens reveal NOTCH regulators suppressing Head and Neck Squamous Cell Carcinoma in mice [Cut&Run]

| PRJNA589895 | ENA

Genome-wide CRISPR Screens in Primary Human T Cells Reveal Key Regulators of Immune Function.

Project description:Human T cells are central effectors of immunity and cancer immunotherapy. CRISPR-based functional studies in T cells could prioritize novel targets for drug development and improve the design of genetically reprogrammed cell-based therapies. However, large-scale CRISPR screens have been challenging in primary human cells. We developed a new method, single guide RNA (sgRNA) lentiviral infection with Cas9 protein electroporation (SLICE), to identify regulators of stimulation responses in primary human T cells. Genome-wide loss-of-function screens identified essential T cell receptor signaling components and genes that negatively tune proliferation following stimulation. Targeted ablation of individual candidate genes characterized hits and identified perturbations that enhanced cancer cell killing. SLICE coupled with single-cell RNA sequencing (RNA-seq) revealed signature stimulation-response gene programs altered by key genetic perturbations. SLICE genome-wide screening was also adaptable to identify mediators of immunosuppression, revealing genes controlling responses to adenosine signaling. The SLICE platform enables unbiased discovery and characterization of functional gene targets in primary cells.

| S-EPMC6689405 | biostudies-literature

Single-cell heterogeneity analysis and CRISPR screens in MIN6 cell line reveal transcriptional regulators of insulin.

Project description:Diabetes mellitus is caused by either insulin resistance or insulin deficiency. The pancreatic β cells are the primary producers of insulin. Large-scale CRISPR screens combined with single-cell RNA sequencing (scRNA-seq) on β cells has identified novel insulin regulators and revealed the presence of a highly complex inner network. Here, we performed pooled CRISPR delivery with single-cell transcriptome analysis on the MIN6 cell line, a pancreatic β-cell line. We have presented the scRNA-seq readout and demonstrated that the MIN6 cell line might develop genetic heterogeneity with increasing passage number based on GO and KEGG pathway analysis. Both computational and biological analyses revealed that the function of MIN6 cell lines could be divided into five clusters, including endocrine cells, basal cells, epithelial cells, and neuroendocrine cells. The fifth cluster was different from the other four clusters due to the differentially expressed insulin transcription and was called the lncRNA-enriched cluster. The experiments also confirmed that uncharacterized lncRNAs GM26917 and Cenpw were associated with insulin transcription. This study provides information that can be used to systematically characterize insulin regulator genes and other genes that control protein folding and vesicle trafficking.

| S-EPMC8565812 | biostudies-literature

CRISPR screens for lipid regulators reveal a role for ER-bound SNX13 in lysosomal cholesterol export.

Project description:We report here two genome-wide CRISPR screens performed to identify genes that, when knocked out, alter levels of lysosomal cholesterol or bis(monoacylglycero)phosphate. In addition, these screens were also performed under conditions of NPC1 inhibition to identify modifiers of NPC1 function in lysosomal cholesterol export. The screens confirm tight coregulation of cholesterol and bis(monoacylglycero)phosphate in cells and reveal an unexpected role for the ER-localized SNX13 protein as a negative regulator of lysosomal cholesterol export and contributor to ER-lysosome membrane contact sites. In the absence of NPC1 function, SNX13 knockdown redistributes lysosomal cholesterol and is accompanied by triacylglycerol-rich lipid droplet accumulation and increased lysosomal bis(monoacylglycero)phosphate. These experiments provide unexpected insight into the regulation of lysosomal lipids and modification of these processes by novel gene products.

| S-EPMC8704955 | biostudies-literature

Genome-wide CRISPR screens of oral squamous cell carcinoma reveal fitness genes in the Hippo pathway.

Project description:New therapeutic targets for oral squamous cell carcinoma (OSCC) are urgently needed. We conducted genome-wide CRISPR-Cas9 screens in 21 OSCC cell lines, primarily derived from Asians, to identify genetic vulnerabilities that can be explored as therapeutic targets. We identify known and novel fitness genes and demonstrate that many previously identified OSCC-related cancer genes are non-essential and could have limited therapeutic value, while other fitness genes warrant further investigation for their potential as therapeutic targets. We validate a distinctive dependency on YAP1 and WWTR1 of the Hippo pathway, where the lost-of-fitness effect of one paralog can be compensated only in a subset of lines. We also discover that OSCCs with WWTR1 dependency signature are significantly associated with biomarkers of favorable response toward immunotherapy. In summary, we have delineated the genetic vulnerabilities of OSCC, enabling the prioritization of therapeutic targets for further exploration, including the targeting of YAP1 and WWTR1.

| S-EPMC7591259 | biostudies-literature

High throughput kinase inhibitor screens reveal TRB3 and MAPK-ERK/TGF? pathways as fundamental Notch regulators in breast cancer.

Project description:Expression of the Notch ligand Jagged 1 (JAG1) and Notch activation promote poor-prognosis in breast cancer. We used high throughput screens to identify elements responsible for Notch activation in this context. Chemical kinase inhibitor and kinase-specific small interfering RNA libraries were screened in a breast cancer cell line engineered to report Notch. Pathway analyses revealed MAPK-ERK signaling to be the predominant JAG1/Notch regulator and this was supported by gene set enrichment analyses in 51 breast cancer cell lines. In accordance with the chemical screen, kinome small interfering RNA high throughput screens identified Tribbles homolog 3 (TRB3), a known regulator of MAPK-ERK, among the most significant hits. We demonstrate that TRB3 is a master regulator of Notch through the MAPK-ERK and TGF? pathways. Complementary in vitro and in vivo studies underscore the importance of TRB3 for tumor growth. These data demonstrate a dominant role for TRB3 and MAPK-ERK/TGF? pathways as Notch regulators in breast cancer, establishing TRB3 as a potential therapeutic target.

| S-EPMC3562766 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data