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Loss of centrosomal gene ALMS1 alters lipid metabolism and the regulation of processes linked to the extracellular matrix.

ABSTRACT: To investigate the alterations that occur in the TGF-B signalling pathway in Alström syndrome, we established by lentiviral transduction with CRISPR an hTERT-BJ-5ta cell line with the ALMS1 gene inhibited. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells (WT and KO) after 24h of TGF-β stimulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE209844 | GEO | 2023/10/31

REPOSITORIES: GEO

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Loss of centrosomal gene ALMS1 alters lipid metabolism and the regulation of processes linked to the extracellular matrix.

Project description:In this project we evaluated the proteomic profiling with TGF-β stimuli at 24h in a CRISPR-Cas9 model for ALMS1 gene in hTERT-BJ-5ta cells. Proteomic results showed a majority inhibition of downstream regulated pathways by the TGF-β, associating the protein coding genes (PCG) with processes like TGF- β matrix regulation, epithelial mesenchymal transition (EMT), PI3K/AKT or P53. In conclusion, seems that the depletion of ALMS1 could be inhibiting the signals transduction through the TGF -β and the routes regulated downstream.

2024-01-26 | PXD035708 | Pride

Loss of the centrosomal protein ALMS1 alters lipid metabolism and the regulation of extracellular matrix-related processes.

Project description:BackgroundAlström syndrome (ALMS) is a rare autosomal recessive disease that is associated with mutations in ALMS1 gene. The main clinical manifestations of ALMS are retinal dystrophy, obesity, type 2 diabetes mellitus, dilated cardiomyopathy and multi-organ fibrosis, characteristic in kidneys and liver. Depletion of the protein encoded by ALMS1 has been associated with the alteration of different processes regulated via the primary cilium, such as the NOTCH or TGF-β signalling pathways. However, the cellular impact of these deregulated pathways in the absence of ALMS1 remains unknown.MethodsIn this study, we integrated RNA-seq and proteomic analysis to determine the gene expression profile of hTERT-BJ-5ta ALMS1 knockout fibroblasts after TGF-β stimulation. In addition, we studied alterations in cross-signalling between the TGF-β pathway and the AKT pathway in this cell line.ResultsWe found that ALMS1 depletion affects the TGF-β pathway and its cross-signalling with other pathways such as PI3K/AKT, EGFR1 or p53. In addition, alterations associated with ALMS1 depletion clustered around the processes of extracellular matrix regulation and lipid metabolism in both the transcriptome and proteome. By studying the enriched pathways of common genes differentially expressed in the transcriptome and proteome, collagen fibril organisation, β-oxidation of fatty acids and eicosanoid metabolism emerged as key processes altered by the absence of ALMS1. Finally, an overactivation of the AKT pathway was determined in the absence of ALMS1 that could be explained by a decrease in PTEN gene expression.ConclusionALMS1 deficiency disrupts cross-signalling between the TGF-β pathway and other dependent pathways in hTERT-BJ-5ta cells. Furthermore, altered cross-signalling impacts the regulation of extracellular matrix-related processes and fatty acid metabolism, and leads to over-activation of the AKT pathway.

| S-EPMC10704752 | biostudies-literature

Loss of centrosomal gene ALMS1 alters lipid metabolism and the regulation of processes linked to the extracellular matrix.

Project description:Loss of centrosomal gene ALMS1 alters lipid metabolism and the regulation of processes linked to the extracellular matrix.

| PRJNA862693 | ENA

H3K9me3 ChIP-Seq in BJ-HELT cells

Project description:We generated H3K9me3 profile of reads and peaks of BJ fibroblasts expressing hTERT and SV40 early region (BJ-HELT cell line).

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miRNA Expression in Senescent and Immortalized BJ fibroblasts

Project description:Limited data exists regarding changes of microRNA (miRNA) expression during senescence in human cells and no reports correlate telomerase expression with regulation of senescence-related miRNAs. We used miRNA microarrays to provide a detailed account of miRNA profiles for early passage and senescent human foreskin (BJ) fibroblasts as well as early and late passage immortalized fibroblasts (BJ-hTERT) that stably express the human telomerase reverse transcriptase subunit hTERT. The revelation that miRNA expression changes with extended passaging in BJ-hTERT cells will contribute to a comprehensive understanding of the connections between telomerase expression, senescence and processes of cellular aging.

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Effect of TERT and ATM on Gene Expression Profiles in Human Fibroblasts

Project description:Gene expression profiling was performed by use of serial analysis of gene expression (SAGE) on BJ normal human skin fibroblasts, A-T cells, and BJ and A-T cells transduced with hTERT cDNA and expressing telomerase activity. Keywords = telomere Keywords = telomerase Keywords = TERT Keywords = ataxia telangiectasia mutated Keywords = ATM Keywords = serial analysis of gene expression Keywords = SAGE Keywords = fibroblast Keywords: parallel sample

2004-01-17 | GSE953 | GEO

Effect of TERT and ATM on Gene Expression Profiles in Human Fibroblasts

2004-01-16 | E-GEOD-953 | biostudies-arrayexpress

Unscheduled HDAC4 repressive activity in human fibroblasts triggers TP53-dependent senescence and favours cell transformation

Project description:In this study we investigated changes in gene expression induced by HDAC4 and RAS in BJ/hTERT LT/ST cells, 48h after the seeding. The goal of the experiment is: a) to find a common signature of transformation between RAS and HDAC4 over-expressing cells; b) to find the peculiarities of the two oncogenic responses.

2019-03-14 | GSE120040 | GEO

Amniocytes (AM) vs. Immortalized AM

Project description:Transcriptional profiling of AM (amniocytes) vs. three different immortalized AM-derived cell lines. Immortalization of AM-derived cell lines by lentiviral vector with hTERT and E6-E7.

2014-12-31 | GSE37615 | GEO

The role of the transcription factors GATA2 and FOXA1 in immortalized basal-like prostate epithelial cells

Project description:GATA2 and FOXA1 are pioneering factors for Androgen Receptor (AR) in prostate cancer cells. Less is known about their role in benign epithelial prostate cells. We investigated if they had the ability to induce differentiation in an undifferentiated prostatic context. Benign basal-like prostate epithelial cells 957E/hTERT-AR cells (a gift from John T. Isaacs lab, Johns Hopkins, MD, USA) were transduced with LentiORF RFP control lentiviral particles. The 957E/hTERT-AR-RFP cells were then transduced with GATA2 and FOXA1 lentiviral particles, and we called the new cell lines hTERT/AR-GATA2 and hTERT/AR-FOXA1, respectively. hTERT/AR-GATA2 is a stable selected cell line and treated with 1 nM anabolic steroids, R1881, or ethanol (ET-OH) for 48 hrs. 957E/hTERT/AR-FOXA1 is a transient cell line, because FOXA1 protein is quickly lost. Twenty four hours post transduction with FOXA1 lentivral particles, 1 nM androgen R1881 or ethanol (ET-OH) were added at time for medium exchange and further treated for 24 hours. GATA-2 and FOXA1 ability to induce differentiation was assessed.

2018-12-01 | E-MTAB-5121 | biostudies-arrayexpress

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