Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The potential biomarkers for HCC patients with functional loss of both p53 and Tsc1

ABSTRACT: p53 mutations occur frequently in human hepatocellular carcinoma (HCC). Activation of the mammalian target of rapamycin (mTOR) pathway is also associated with HCC. However, it is still unknown whether these changes together initiate HCC and can be targeted as a potential therapeutic strategy. Here, we compared transcriptional profiles among a panel of liver tissue samples from p53+/-, Tsc1fl/fl;Alb-cre, and p53+/-;Tsc1fl/fl;Alb-cre mice by RNAseq analysis. The overlapping genes in those three genotypes were considered potential biomarkers for HCC patients with functional loss of both p53 and Tsc1.

ORGANISM(S): Mus musculus

PROVIDER: GSE153223 | GEO | 2021/08/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Tsc1 promotes the differentiation of memory CD8+ T cells via orchestrating the transcriptional and metabolic programs

Project description:Memory CD8+ T cells are an essential component of protective immunity. Signaling via mechanistic target of rapamycin (mTOR) has been implicated in the regulation of the differentiation of effector and memory T cells. However, little is understood about the mechanisms that control mTOR activity, or the effector pathways regulated by mTOR, in this process. We describe here that tuberous sclerosis 1 (Tsc1), a regulator of mTOR signaling, plays a crucial role in promoting the differentiation and function of memory CD8+ T cells in response to Listeria monocytogenes infection. Mice with specific deletion of Tsc1 in antigen-experienced CD8+ T cells evoked normal effector responses, but were markedly impaired in the generation of memory T cells and their recall responses to antigen re-exposure in a cell-intrinsic manner. Tsc1 deficiency suppressed the generation of memory-precursor effector cells (MPECs) while promoting short-lived effector cell (SLEC) differentiation. Functional genomic analysis indicated that Tsc1 coordinated gene expression programs underlying immune function, transcriptional regulation and cell metabolism. Furthermore, Tsc1 deletion led to excessive mTORC1 activity and dysregulated cellular metabolism including glycolytic and oxidative metabolism. These findings establish a Tsc1-mediated checkpoint in linking immune signaling and cell metabolism to orchestrate memory CD8+ T cell development and function. We used microarrays to explore the gene expression profiles differentially expressed in OVA-specific CD8+ T-cells from wild-type (WT; Tsc1-fl/fl and cre-negative) and Tsc1-/- (Tsc1-fl/fl and Granzyme B-cre-positive) mice

2014-09-20 | E-GEOD-61591 | biostudies-arrayexpress

Comprehensive proteometics identifies FBXL6 substrates involved in liver cancer

Project description:FBXL6 is frequently over-expressed in human hepatocellular carcinoma (HCC). However, it is still unknown the underlying mechanisms by which FBXL6 promotes HCC. In this study, we compared ubiquitinated protein profiles among a panel of liver tissue samples (including HCC, adjacent tissues and normal tissues) from Fbxl6LSL-fl/+; Alb-cre mice and Alb-cre mice by proteomics and ubiquitomics analysis. There are many proteins with ubiquitination in FBXL6 overexpressed HCC, suggesting ubiquitination may play a critical role in FBXL6-mediated HCC. A1--- normal tissue 1 A2--- normal tissue 2 B1--- Adjacent tissue 1 B2--- Adjacent tissue 2 C1--- HCC tissue 1 C2--- HCC tissue 2

2024-01-26 | PXD032357 | Pride

The potential biomarkers for HCC patients with functional loss of both p53 and Tsc1

Project description:The potential biomarkers for HCC patients with functional loss of both p53 and Tsc1

| PRJNA641801 | ENA

Microarray analysis of WT, SKO, PKO and DKO liver samples

Project description:Microarray analysis of WT (Pten2fl/fl:Shp2fl/fl:Alb-Cre-), SKO (Shp2hep-/-, or Shp2fl/fl:Alb-Cre+), PKO (Ptenhep-/-, or Pten2fl/fl:Alb-Cre+) and DKO (Ptenfl/fl:Shp2fl/fl:Alb-Cre+) liver samples to gain global molecular insights how shp2 and pten is involved in liver tumorigenesis.

2016-12-13 | GSE74732 | GEO

Met Expression Signature in Hepatocytes

Project description:To identify HGF/Met regulated genes, we performed expression microarray analysis after inducible activation of Met receptor in primary cultures of hepatocytes established from wild-type control (Alb-Cre +/-) and Met conditional knockout mice (Alb-Cre +/-; Met Fl/Fl). Keywords: time series design

2006-10-02 | GSE4451 | GEO

Rapamycin effect on Wild Type and TSC deficient Mouse Embryonic Fibroblasts : Time Course

Project description:Aberrant activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a common molecular event in a large variety of pathological settings, including genetic tumor syndromes, cancer, and obesity. However, the cell intrinsic consequences of mTORC1 activation remain poorly defined. Here, we identify global trancriptional changes in TSC1 and TSC2 null MEFs, which exhibit constitutive activation of mTORC1, compared to wild-type littermate control lines. A rapamycin time course is included to determine those changes that are dependent on mTORC1 signaling, revealing mTORC1 induced and repressed transcripts. In order to identify mTORC1-dependent transcriptional changes, we compared wild-type MEFs to both Tsc1-/- and Tsc2-/- MEFs following serum starvation, where mTORC1 signaling is off in wild-type cells and fully active in TSC-deficient cells. All cell lines were serum-starved for 24 h, and the Tsc1-/- and Tsc2-/- cells were treated with a time course of rapamycin prior to the isolation of mRNA for microarray analysis. Immortalized wild-type (Tsc2+/+ p53-/-), Tsc1-/- (p53+/+, 3T3-immortalized), and Tsc2-/- (p53-/-, derived from a littermate of the wild-type cell line) MEFs are the three cell lines used in this study and were derived in the laboratory of David J. Kwiatkowski (Brigham and Women's Hospital, Harvard Medical School, Boston, MA). Wild-type and null MEFs were grown to 70% confluence in 10 cm plates and were serum starved for 24 h in the presence of vehicle (DMSO) for 24 h or rapamycin (20 nM) for 2, 6, 12, or 24 h. All vehicle-treated samples (0 h time points) were plated in triplicate and all rapamycin time course samples were plated in duplicate. For each replicate, expression analysis was performed by hybridization to an Affymetrix Mouse 430_2 oligonucleotide microarray chip.

2010-07-30 | E-GEOD-21755 | biostudies-arrayexpress

IκBζ Regulates the Development of Nonalcoholic Fatty Liver Disease through the Attenuation of Hepatic Steatosis in Mice

Project description:IκBζ is a transcriptional regulator that augments inflammatory responses from the Toll-like receptor or interleukin signaling. These innate immune responses contribute to the progression of nonalcoholic fatty liver disease (NAFLD); however, the role of IκBζ in the pathogenesis of NAFLD remains elusive. We investigated whether IκBζ was involved in the progression of NAFLD in mice. We generated hepatocyte-specific IκBζ-deficient mice (Alb-Cre; Nfkbizfl/fl) by crossing Nfkbizfl/fl mice with Alb-Cre transgenic mice. NAFLD was induced by feeding the mice a choline-deﬁcient, L-amino acid-deﬁned, high-fat diet (CDAHFD). CDAHFD-induced IκBζ expression in the liver was observed in Nfkbizfl/fl mice, but not in Alb-Cre; Nfkbizfl/fl mice. Contrary to our initial expectation, IκBζ deletion in hepatocytes accelerated the progression of NAFLD after CDAHFD treatment. Although the increased expression of inflammatory cytokines and apoptosis-related proteins by CDAHFD remained unchanged between Nfkbizfl/fl and Alb-Cre; Nfkbizfl/fl mice, early-stage steatosis of the liver was significantly augmented in Alb-Cre; Nfkbizfl/fl mice. Overexpression of IκBζ in hepatocytes via the adeno-associated virus vector attenuated liver steatosis caused by the CDAHFD in wild-type C57BL/6 mice. This preventive effect of IκBζ overexpression on steatosis was not observed without transcriptional activity. Microarray analysis revealed a correlation between IκBζ expression and the changes of factors related to triglyceride biosynthesis and lipoprotein uptake. Our data suggest that hepatic IκBζ attenuates the progression of NAFLD possibly through the regulation of the factors related to triglyceride metabolism.

2022-06-05 | GSE205390 | GEO

Genome-wide analysis of livers of control and Lats1/2 deficient neonatal mice [Microarray expression]

Project description:Lats1-/-;Lats2fl/fl;Alb-Cre pups and control pups were sacrificed at 1 day after birth

2016-06-29 | GSE71872 | GEO

Melanoma Differentiation Associated Gene-9/Syndecan Binding Protein (MDA-9/SDCBP) Promotes Hepatocellular Carcinoma (HCC)

Project description:The oncogene Melanoma differentiation associated gene-9/syndecan binding protein (MDA-9/SDCBP) promotes tumorigenesis and metastasis in many cancers. However, the role of MDA-9 in regulating HCC has not been well-studied. To unravel the function of MDA-9 in HCC we generated a transgenic mouse with hepatocyte-specific overexpression of MDA-9 (Alb/MDA-9). Alb/MDA-9 mice demonstrated significantly higher incidence of N-nitrosodiethylamine/phenobarbital-induced HCC compared to WT littermates. To check what genes are regulated by MDA-9 to promote HCC, RNA-seq was performed in naïve WT and Alb/MDA-9 hepatocytes.

2023-12-27 | GSE199175 | GEO

Genome-wide profiling for H2A.Z and genome accessibility using ATACseq in Uhrf1hepKO mouse livers compared to WT livers

Project description:This study was carried out to investigate potential changes in the genome-wide distribution of H2AZ and genome accessibility using ATACseq in livers where Uhrf1 is deleted in hepatocytes (Uhrf1-fl/fl;Alb:Cre) compared to controls (Uhrf1-fl/fl).

2020-07-17 | GSE153090 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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