Dataset Information

CRISPR-Cas9-mediated ALMS1 knockout inhibits TGF-β signalling and epithelial-mesenchyme transition.

ABSTRACT: In this project we evaluated the proteomic profiling with TGF-β stimuli at 24h in a CRISPR-Cas9 model for ALMS1 gene in HeLa cells. Proteomic results showed a majority inhibition of downstream regulated pathways by the TGF-β, associating the protein coding genes (PCG) with processes like focal adhesion or cell-substrate adherens junction. Finally, EMT biomarkers like VIM, DSP, EDIL3 and SNAI1 had the opposite pattern to what would be expected when activating the EMT. In conclusion, seems that the depletion of ALMS1 could be inhibiting the signals transduction through the TGF -β and the routes regulated downstream by it such as the EMT.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Cervical Adenocarcinoma

SUBMITTER: Brais Bea Mascato

LAB HEAD: Diana Valverde Pérez

PROVIDER: PXD024964 | Pride | 2023-03-11

REPOSITORIES: Pride

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Depletion of ALMS1 affects TGF-β signalling pathway and downstream processes such as cell migration and adhesion capacity.

Bea-Mascato Brais B Neira-Goyanes Elena E Iglesias-Rodríguez Antía A Valverde Diana D

Frontiers in molecular biosciences 20221013

Background: ALMS1 is a ubiquitous gene associated with Alström syndrome (ALMS). The main symptoms of ALMS affect multiple organs and tissues, generating at last, multi-organic fibrosis in the lungs, kidneys and liver. TGF-β is one of the main pathways implicated in fibrosis, controlling the cell cycle, apoptosis, cell migration, cell adhesion and epithelial-mesenchymal transition (EMT). Nevertheless, the role of ALMS1 gene in fibrosis generation and other implicated processe ...[more]

PMID: 36325276

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Project description:Our group is interested in epithelial-to-mesenchymal transition (EMT), in particular, TGF-beta induced EMT. TGF-beta signalling has been shown to be an important factor in the induction of EMT and it has been demonstrated that adding TGF-beta to epithelial cells in culture is a convenient way to study the process of EMT. In response to TGF-beta, Smad2 and 3 are activated, and form complexes with Smad4, which then regulate transcription of target genes through interactions with other DNA binding transcription factors. In the induction of EMT, the activated Smads mediate transcriptional regulation through three families of transcription factors, resulting in repression of epithelial marker gene expression and activation of mesenchymal gene expression (Xu J, et al. 2009) Also investigated in this study is the role of H2A.Z in EMT. H2A.Z is an evolutionary conserved and a metazoan essential histone variant of the H2A class. Mice deficient in H2A.Z die during early development but the reason for this is unknown (Faast et al. 2001). Previously, our laboratory showed that the loss of H2A.Z in Xenpous laevis impaired cell movement required for the formation of the mesoderm and neural crest (Ridgway et al. 2004). Given that mesoderm formation is critically dependent upon EMT, we therefore wondered whether H2A.Z might be a chromatin regulator of EMT. We transfected MDCK cells with a lentiviral vector to express a construct encoding an shRNA targeting canine H2A.Z as we wanted to test the hypothesis that H2A.Z is involved in the maintenance of cellular identity and that its loss might trigger de-differentiation. In order to investigate changes in histone variant H2A.Z occupancy associated with TGF-beta induced epithelial-to-mesenchymal transition (EMT) we performed H2A.Z ChIP-Seq in untreated and TGFb-treated MDCK cells. The MDCK cell line has been extensively used as a model system for EMT because they convert fully from the epithelial to the mesenchymal state in response to TGF-beta. Please note that RNA-seq data generated in conjunction to this ChIP-seq data set were also deposited at ArrayExpress under accession number E-MTAB-5628 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5628 ).

			Action	DRS
	DVPDVO340128_Gel.pptx	Other
	DVPDVP340128.dta.zip	Other
	DVPDVP340128.mgf	Mgf
	DVPDVP340128.msf	Msf
	DVPDVP340128.pep.pep.xml	Pepxml

Dataset Information

CRISPR-Cas9-mediated ALMS1 knockout inhibits TGF-β signalling and epithelial-mesenchyme transition.

Dataset's files

Publications

Depletion of <i>ALMS1</i> affects TGF-β signalling pathway and downstream processes such as cell migration and adhesion capacity.

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