Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SMAD4 lossdifferentlyshapespancreatictumorswithdistinct KRASmutations

ABSTRACT: We compared KPC Smad4 WT and Smad4 KO tumours from orthotopically-grafted organoid-derived mouse models

ORGANISM(S): Mus musculus

PROVIDER: GSE274684 | GEO | 2024/12/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-sea of Smad4 wild-type or Smad4 knockout KPC PDAC organoids from monocultures or co-cultures with pancreatic stellate cells and RNA-seq of flow-sorted PSCs from the same co-cultures.

Project description:RNA-sequencing of flow-sorted Smad4 wild-type (WT) or Smad4 knockout (KO) KPC (i.e. KRASG12D; p53 mutant) pancreatic ductal adenocarcinoma (PDAC) organoids from monocultures or co-cultures with pancreatic stellate cells (PSCs) and RNA-sequencing of flow-sorted PSCs from the same co-cultures. We investigated changes in transcriptome in Smad4 KO KPC PDAC organoids compared to Smad4 WT KPC PDAC organoids in monoculture or in co-culture with PSCs. We also investigated the changes in transcriptome in PSCs co-cultured with Smad4 WT or Smad4 KO KPC PDAC organoids.

2024-12-02 | GSE263080 | GEO

RNA-sea of Smad4 wild-type or Smad4 knockout KvPC PDAC organoids from monocultures or co-cultures with pancreatic stellate cells and RNA-seq of flow-sorted PSCs from the same co-cultures.

Project description:RNA-sequencing of flow-sorted Smad4 wild-type (WT) or Smad4 knockout (KO) KvPC (i.e. KRASG12V; p53 mutant) pancreatic ductal adenocarcinoma (PDAC) organoids from monocultures or co-cultures with pancreatic stellate cells (PSCs) and RNA-sequencing of flow-sorted PSCs from the same co-cultures. We investigated changes in transcriptome in Smad4 KO KvPC PDAC organoids compared to Smad4 WT KvPC PDAC organoids in monoculture or in co-culture with PSCs. We also investigated the changes in transcriptome in PSCs co-cultured with Smad4 WT or Smad4 KO KvPC PDAC organoids.

2024-12-02 | GSE263081 | GEO

Single-cell RNA-sequencing of murine pancreatic tumors derived from the orthotopic transplantation of Smad4 wild-type (WT) or Smad4 knockout (KO) pancreatic ductal adenocarcinoma (PDAC) KPC organoids in nu/nu mice.

Project description:We investigated the effect of SMAD4 loss in KPC PDAC tumors

2024-12-24 | GSE262879 | GEO

Expression analysis of SPDEF KO and hRosa26 clones of hF27, CFPAC1 and HPAF-II orthotopically grafted into the pancreata of NSG mice.

Project description:This study used Illumina RNA-sequencing to examine gene expression differences following Spdef deletion in hF27, CFPAC1 and HPAF-II orthotopically grafted tumor models.

2024-01-25 | GSE211348 | GEO

The tumor suppressor SMAD4 acts through WNT signaling in progression from benign lesions to oral squamous cell carcinoma

Project description:SMAD4 is a tumor suppressor mutated or silenced in multiple cancers including oral squamous cell carcinoma (OSCC). Human clinical samples and cell lines, mouse models and organoid culture were used to investigate the role that SMAD4 plays in progression from benign disease to invasive OSCC. Human OSCC lost detectable SMAD4 protein within tumor epithelium in 24% of cases and this loss correlated with worse progression free survival independent of other major clinical and pathological features. In a mouse model, Kras mutation induced benign papillomas while additional loss of Smad4 expression resulted in rapid development of invasive carcinoma. Examining regulatory pathways in organoids from SMAD4+ and SMAD4- mouse tumors, we found that either loss of SMAD4 or inhibition of TGFb signaling upregulated the WNT pathway and altered the extracellular matrix. The gene signature of the mouse tumor organoids lacking SMAD4 was highly similar to the gene signature of human head and neck squamous cell carcinoma. In summary, this work has uncovered novel mechanisms by which SMAD4 acts as a tumor suppressor in OSCC.

2024-05-14 | GSE228584 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and SMAD4 Y95 Mutation Transcriptomes

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of Y95 phosphorylation on SMAD4-mediated transcription in response to TGF-b signals. The goals of this study are to compare transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Methods: mRNA profiles of HaCaT parental and SMAD4 KO cells stably expressing wild-type SMAD4 (WT), Y95E or Y95F mutant, and GFP (as control) under with or without TGF-b were generated by deep sequencing, using Illumina HiSeq X Ten. qRT–PCR validation was performed using TaqMan and SYBR Green assays Conclusions: hierarchical clustering of the global gene expression profiles of TGF-β treated cells revealed that wild-type-SMAD4- and Y95F-mutant-rescued SMAD4-null cells were highly similar to the parental HaCaT cells, whereas GFP- and Y95E-mutant-rescued cells formed a separate cluster

2018-10-22 | GSE121188 | GEO

Smad4 and Trim33 dependend nodal/activin responsive genes in differentiated mouse ESCs

Project description:In differentiated mouse ESCs, most of the nodal/activin responsive genes are dependent on both Smad4 and Trim33, some are solely dependent on Smad4, and some are dependent on Trim33. Ebs at Day2.5 from WT, Smad4 null, and Trim33 knock-down ESCs, were treated with activin or SB 431542 for 2 h.

2012-01-09 | E-GEOD-32903 | biostudies-arrayexpress

Smad4 restricts injury-provoked biliary proliferation and carcinogenesis (AKPS_EV_vs_Smad4_MethylSeq)

Project description:Reduced representation bisulfite sequencing (RRBS) on the same TGFβ-treated AKPS lines (with EV or Smad4) revealed that Smad4 impacts DNA methylation (DNAme), with decreases in intergenic DNAme as the most impacted in our CCA models.

2023-12-07 | GSE237680 | GEO

A Pancreas Organoids-based Screen Identifies a Specific KRAS Mutation Inhibitor that Attenuating Cholesterol Biosynthesis Pathway in Pancreatic Cancer

Project description:we reported a high-content drug screening platform of a series of pancreas organoids which contain common mutations found in human pancreatic cancer, wide type (WT), KC (KRASG12D), KPC (KRASG12D; Tp53R172H), KSC (KRASG12D; SMAD4-/-) and KPSC (KRASG12D; Tp53R172H and SMAD4-/-). Based on this platform, we screened about 6000 compounds and identified Perhexiline, which can inhibit the growth of pancreas organoids with KRAS mutation in vitro and in vivo. Single cell RNA-seq data shows that the cholesterol synthesis pathway is activated specifically caused by KRAS in mutated organoid lines. The key cholesterol synthesis regulator of SREBP2 and its downstream genes are activated in KRAS mutated organoids compared with WT. Interestingly, Perhexiline can reverse the metabolism changes in pancreas organoids with KRAS through downregulating SREBP2 at transcription level. Finally, we further validated targeting SREBP2 can attenuate tumor growth significantly with chemical inhibitor and genetic perturbation. These findings boost further understanding of KRAS in PDAC and provide a valuable resource for targeting KRAS therapeutics development.

2023-11-16 | GSE207352 | GEO

Pancreatic cancer organoid

Project description:Organoids from KPC pancreatic tumor tissue was treated with growth medium or conditional medium of mast cells treated with WT or BAG6 KO EVS of Pan02.

2024-12-31 | E-MTAB-13570 | biostudies-arrayexpress

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