Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global gene expression of histologically normal primary skin cells from BCNS subjects reveals “single-hit” effects that are influenced by rapamycin

ABSTRACT: Global gene expression of histologically normal primary skin cells from BCNS subjects reveals “single-hit” effects that are influenced by rapamycin

PROVIDER: PRJNA492292 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Global gene expression of histologically normal primary skin cells from BCNS subjects reveals "single-hit" effects that are influenced by rapamycin.

Project description:Studies of dominantly heritable cancers enabled insights about tumor progression. BCNS is a dominantly inherited disorder that is characterized by developmental abnormalities and postnatal neoplasms, principally BCCs. We performed an exploratory gene expression profiling of primary cell cultures derived from clinically unaffected skin biopsies of BCNS gene-carriers (PTCH1 +/-) and normal individuals. PCA and HC of untreated keratinocytes or fibroblasts failed to clearly distinguish BCNS samples from controls. These results are presumably due to the common suppression of canonical HH signaling in vitro. We then used a relaxed threshold (p-value <0.05, no FDR cut-off; FC 1.3) that identified a total of 585 and 857 genes differentially expressed in BCNS keratinocytes and fibroblasts samples, respectively. A GSEA identified pancreatic β cell hallmark and mTOR signaling genes in BCNS keratinocytes, whereas analyses of BCNS fibroblasts identified gene signatures regulating pluripotency of stem cells, including WNT pathway. Significantly, rapamycin treatment (FDR<0.05), affected a total of 1411 and 4959 genes in BCNS keratinocytes and BCNS fibroblasts, respectively. In contrast, rapamycin treatment affected a total of 3214 and 4797 genes in normal keratinocytes and normal fibroblasts, respectively. The differential response of BCNS cells to rapamycin involved 599 and 1463 unique probe sets in keratinocytes and fibroblasts, respectively. An IPA of these genes in the presence of rapamycin pointed to hepatic fibrosis/stellate cell activation, and HIPPO signaling in BCNS keratinocytes, whereas mitochondrial dysfunction and AGRN expression were uniquely enriched in BCNS fibroblasts. The gene expression changes seen here are likely involved in the etiology of BCCs and they may represent biomarkers/targets for early intervention.

| S-EPMC6402716 | biostudies-literature

Global gene expression of histologically normal primary skin cells from BCNS subjects reveals “single-hit” effects that are influenced by rapamycin

Project description:The study of dominantly heritable cancers has provided significant insights about tumor development. Basal cell nevus syndrome (BCNS), or Gorlin syndrome (OMIM #109400), is an autosomal dominant inherited disorder that is characterized by developmental abnormalities and postnatal occurrence of various neoplasms, principally basal cell carcinomas (BCCs). We performed an exploratory gene expression profiling of primary cultures, including keratinocytes and fibroblasts derived from clinically unaffected skin biopsies of BCNS gene-carriers (PTCH1 +/-) and normal individuals.

2019-03-20 | GSE120242 | GEO

Comparing effects of rapamycin and caffeine on gene expression in YPD media

Project description:To identify genes influenced by rapamycin and caffeine in strains W303a, S288c, and Sigma 2000 Keywords: Drug dose response

2006-04-04 | GSE4584 | GEO

Hydropsychidae Influenced Microbiomes

Project description:Hydropsychidae Influenced Microbiomes Metagenome

| PRJNA834817 | ENA

Chromatin footprints after double-hit stress

Project description:It was our goal to discern the epigenomic signatures of the ventral hippocampus, in male and female mice in a double hit model of acute stress: one hit of acute restraint stress followed by forced swim stress one week later.

2022-06-20 | GSE200670 | GEO

Influenced genes by miR663a

Project description:Influenced genes by miR663a

| PRJNA483738 | ENA

Ornithogenically influenced soil samples

Project description:Ornithogenically influenced soil samples Metagenome

| PRJNA1025294 | ENA

Chromatin footprints after double-hit stress

Project description:Chromatin footprints after double-hit stress

| PRJNA825824 | ENA

Rapamycin With Grapefruit Juice for Advanced Malignancies

Project description:The purpose of this study is to determine the highest safe dose of rapamycin when given with a fixed amount of grapefruit juice.

| 2032603 | ecrin-mdr-crc

Modulation of nonsense-mediated decay by rapamycin

Project description:Rapamycin is a naturally occurring macrolide whose target is at the core of nutrient and stress regulation in a wide range of species. Despite well-established roles as an inhibitor of cap-dependent mRNA translation, relatively little is known about its effects on other modes of RNA processing. Here, we characterize the landscape of rapamycin-induced post-transcriptional gene regulation. Transcriptome analysis of rapamycin-treated cells revealed genome-wide changes in alternative mRNA splicing and pronounced changes in NMD-sensitive isoforms. We demonstrate that despite well-documented attenuation of cap-dependent mRNA translation, rapamycin can augment NMD of certain transcripts. Rapamycin-treatment significantly reduces the levels of both endogenous and exogenous PTC-containing mRNA isoforms and its effects are dose-, UPF1- and 4EBP-dependent manner. The PTC-containing SRSF6 transcript exhibits a shorter half-life upon rapamycin-treatment as compared to the non-PTC isoform. Rapamycin-treatment also caused depletion of PTC-containing mRNA isoforms from polyribosomes, underscoring the functional relationship between translation and NMD. Enhanced NMD activity also correlates with an enrichment of the nuclear Cap Binding Complex (CBC) in rapamycin-treated cells. Our data demonstrate that rapamycin modulates global RNA homeostasis by NMD.

2016-11-11 | GSE89774 | GEO

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