Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer

ABSTRACT: CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer

PROVIDER: PRJNA579893 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10353932.fastq.gz	Fastqsanger.gz
	SRR10353933.fastq.gz	Fastqsanger.gz
	SRR10353934.fastq.gz	Fastqsanger.gz
	SRR10353935.fastq.gz	Fastqsanger.gz
	SRR10353936.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer

Project description:Small cell lung cancer (SCLC) is a highly aggressive subtype of lung cancer that remains among the most lethal of solid tumor malignancies. Recent genomic sequencing studies have identified many recurrently mutated genes in human SCLC tumors. However, the functional roles of most of these genes remain to be validated. Here, we adapt the CRISPR-Cas9 system to a well-established murine model of SCLC to rapidly model loss-of-function mutations in candidate genes identified from SCLC sequencing studies. We show that loss of the gene p107 significantly accelerates tumor progression. Notably, compared with loss of the closely related gene p130, p107 loss results in fewer but larger tumors, as well as earlier metastatic spread. In addition, we observe differences in proliferation and apoptosis, as well as altered distribution of initiated tumors in the lung, resulting from loss of p107 or p130. Collectively, these data demonstrate the feasibility of using the CRISPR-Cas9 system to model loss of candidate tumor suppressor genes in SCLC, and we anticipate that this approach will greatly facilitate efforts to investigate mechanisms driving tumor progression in this deadly disease.

2019-12-19 | GSE139444 | GEO

Somatic CRISPR/Cas9-mediated tumor suppressor disruption enables versatile murine cancer modeling

Project description:Recent cancer genome sequencing studies have identified numerous novel candidate driver genes. In vivo functional investigation of oncogenes using somatic gene transfer has been successfully exploited as a versatile means to validate their pathogenic relevance. In contrast, such functional analyses have been hampered for candidate tumor suppressor genes, e.g. by insufficient knockdown using RNAi-mediated approaches. In order to provide a flexible method for investigating loss-of-function mutations and their potential role in tumorigenesis, we have established CRISPR/Cas9-mediated somatic gene disruption, allowing for in vivo deletion of candidate tumor suppressor genes. We demonstrate the utility of this approach by somatic disruption of the Ptch1 gene in the mouse cerebellum, leading to the formation of medulloblastoma faithfully resembling the SHH-driven subgroup of the disease. This in vivo method for validation of candidate tumor suppressor genes provides a fast and convenient system for the generation of faithful animal models of human cancer.

2014-12-31 | GSE58629 | GEO

CRISPR/Cas9-mediated validation of candidate Master Regulators Proteins in DMG/GBM Cell Lines

Project description:CRISPR/Cas9-mediated validation of candidate Master Regulators Proteins in DMG/GBM Cell Lines

| PRJNA1111466 | ENA

CRISPR/Cas9-mediated validation of candidate Master Regulators Proteins in DMG/GBM Cell Lines

Project description:Three GBM and three DMG cell lines were selected to be used in a function validation CRISPR screening to elucidate essentiality of canidate Master Regulator proteins

2025-12-22 | GSE267415 | GEO

CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer.

Project description:Small cell lung cancer (SCLC) is a highly aggressive subtype of lung cancer that remains among the most lethal of solid tumor malignancies. Recent genomic sequencing studies have identified many recurrently mutated genes in human SCLC tumors. However, the functional roles of most of these genes remain to be validated. Here, we have adapted the CRISPR-Cas9 system to a well-established murine model of SCLC to rapidly model loss-of-function mutations in candidate genes identified from SCLC sequencing studies. We show that loss of the gene p107 significantly accelerates tumor progression. Notably, compared with loss of the closely related gene p130, loss of p107 results in fewer but larger tumors as well as earlier metastatic spread. In addition, we observe differences in proliferation and apoptosis as well as altered distribution of initiated tumors in the lung, resulting from loss of p107 or p130 Collectively, these data demonstrate the feasibility of using the CRISPR-Cas9 system to model loss of candidate tumor suppressor genes in SCLC, and we anticipate that this approach will facilitate efforts to investigate mechanisms driving tumor progression in this deadly disease.

| S-EPMC6955235 | biostudies-literature

Validation Study for Candidate AD miRNA Biomarkers in Human CSF

Project description:Validation Study for Candidate AD miRNA Biomarkers in Human CSF

| PRJNA876275 | ENA

ALDH1A2 Is a Candidate Tumor Suppressor Gene in Ovarian Cancer”

Project description:ALDH1A2 Is a Candidate Tumor Suppressor Gene in Ovarian Cancer”

| PRJNA559144 | ENA

Prediction and validation of a human immunodeficiency with CRISPR

Project description:Prediction and validation of a human immunodeficiency with CRISPR

| PRJNA1028553 | ENA

G6PC3 promotes genome maintenance and is a candidate mammary tumor suppressor

Project description:G6PC3 promotes genome maintenance and is a candidate mammary tumor suppressor

| PRJNA1170348 | ENA

Probing the Tumour Suppressor Function of BAP1 in CRISPR-engineered Human Liver Organoids

Project description:The deubiquitinating enzyme BAP1 is a tumour suppressor, amongst others involved in cholangiocarcinoma. BAP1 has many proposed molecular targets, while its Drosophila homolog is known to deubiquitinate Histone H2AK119. Here, we mutate BAP1 by CRISPR/Cas9 in normal human liver organoids. We find that BAP1 controls the expression of junctional/cytoskeleton components by regulating chromatin accessibility. Consequently, we observe loss of multiple epithelial characteristics, while motility increases. Importantly, restoring the catalytic activity of BAP1 in the nucleus rescues these cellular and molecular changes. We engineer human liver organoids to combine four common cholangiocarcinoma mutations (TP53, PTEN, SMAD4, NF1). In this genetic background, BAP1 loss results in acquisition of malignant features upon xenotransplantation. Thus, control of epithelial identity through the regulation of chromatin accessibility appears a key aspect of BAP1’s tumour suppressor function. Organoid technology combined with CRISPR/Cas9 provides an experimental platform for mechanistic studies of cancer gene function in a human context.

2019-05-22 | PXD013353 | Pride

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