Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single Cell RNA Sequencing of MIC WT and B1KO early invasive breast carcinoma

ABSTRACT: The goal of this study is the compare the tumour compositions between B1 integrin-proficient and -deficient dormant lesions based on single cell transcripts. Tumours were dissociated and pooled into single cell suspension, passed multi-stage quality checks, and sequenced by Génome Québec Innovation Tumour. Clustering visualization by UMAP and differential gene expression analyses show that B1 integrin-deficient dormant lesions have significantly more cancer-associated fibroblasts by depleted of antitumourigenic immune cells, altogether promoting dormnacy exit and recurrence.

ORGANISM(S): Mus musculus

PROVIDER: GSE186118 | GEO | 2021/10/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

b1 integrin regulates epithelial proliferation and cell shape during alveolar repair

Project description:Integrins are extracellular matrix receptors comprised of an a and b subunit that connect and mediate signaling between cells and the surrounding matrix. In organogenesis of epithelial tissues, the b1 integrin subunit regulates essential epithelial cell functions, but the role of b1 integrin in epithelial repair is poorly understood. To define the role of b1 integrin during alveolar repair, we challenged b1 integrin deficient mice with intratracheal lipopolysaccharide, resulting in increased mortality with emphysematous lungs 21 days following injury. The alveolar barrier was repopulated with an overabundance of type 2 alveolar epithelial cells, with reduced numbers of elongated alveolar type 1 cells, suggesting b1 integrin is required for type 2 to type 1 epithelial transition. Consistent with this finding, b1 deficient type 2 epithelial cells proliferated at increased rates throughout repair, lacked actin-rich cellular protrusions necessary for lateral cellular extension, and exhibited transcriptomic dysregulation of adherens junction and actin polymerization pathways. Finally, we show that b1 integrin balances actin polymerization versus stabilization through GTPase activation. Taken together, these data support a novel role for b1 integrin in re-establishing the alveolar niche after injury through modulation of type 2 epithelial cell proliferation and cytoskeletal-dependent cell shape change.

2023-06-10 | GSE205882 | GEO

b1-integrin regulates marginal zone B cell differentiation

Project description:Integrin b1-deficient mice have a defect in the differentiation of MZ B cells and plasma cells.We performed a genome-wide transcriptome analysis of ex vivo-sorted Fo B, transitional B and MZ B cells of in Integrin b1 KO and Integrin b1 WT mice. We also performed invitro culture of CD93+ (AA4.1+) transitional B cells to study the role of PI3 Kinase signalling.

2022-09-19 | GSE213512 | GEO

Ligand-independent integrin beta1 signaling supports lung adenocarcinoma development

Project description:Integrins, the principal extracellular matrix (ECM) receptors of the cell, promote cell adhesion, migration, and proliferation, which are key events for cancer growth and metastasis. To date, most integrin-targeted cancer therapeutics have disrupted integrin-ECM interactions, which are viewed as critical for integrin functions. However, such agents have failed to improve cancer patient outcomes. We show that integrin b1, a highly expressed subunit in lung epithelium, is required for lung adenocarcinoma development in a carcinogen-induced mouse model. Likewise, human lung adenocarcinoma cell lines with integrin b1 deletion failed to form colonies in soft agar and tumors in mice. Mechanistically, we demonstrate that these effects do not require integrin b1-mediated adhesion to ECM but are dependent on integrin b1 cytoplasmic tail-mediated activation of focal adhesion kinase (FAK). Together, these studies support a critical role for integrin b1 in lung tumorigenesis that is mediated through constitutive, ECM-binding independent signaling involving the cytoplasmic tail.

2022-08-01 | GSE175687 | GEO

The effect of aneuploidy on gene expression

Project description:Analysis of the gene expression changes observed in aneuploid b1 integrin YYFF MEFs generated as a result of repeated cytokinesis failure compared to tetraploid wild-type MEFs or tetraploid b1YYFF integrin MEFs. The results reveal aneuploidy-specific gene expression changes, both up-and downregulated genes uniquely detected in the aneuploid MEFs. Total RNA isolated from b1 integrin YYFF and B1 wildtype mouse embryonic fibroblasts that had been passaged on laminin 0, 4 or 8 times (L0, L4 or L8)

2013-07-02 | E-GEOD-23729 | biostudies-arrayexpress

Integrin b1 acetylation-induced transcriptomic reprograming of mouse embryonic endothelial cells and functions

Project description:Reciprocal regulation of integrin-dependent cell-matrix adhesions and cell-cell junctions is critical for controlling endothelial permeability and proliferation in cancer and inflammatory diseases, but remain poorly understood. Here, we investigated how acetylation of the distal NPKY-motif of b1-integrin influences endothelial cell physiology and barrier function. Expression of an acetylation-mimetic B1A-K794Q-GFP mutant induced transcriptomic reprograming of embryonic endothelial cells particularly in genes responsible for cell adhesion, proliferation, polarity and barrier function. B1A-K794Q-GFP induced a constitutive activation of MAPK signaling, an impairment of junctions, increased proliferation and an altered contact inhibition at confluency. Structural analysis of integrin b1 interaction with KINDLIN-2, biochemical pulldown assay and molecular dynamic analysis showed that acetylation of K794 increases KINDLIN-2 binding to the integrin b1 cytoplasmic tail. Accordingly, altering KINDLIN-2 levels modified Claudin-5 expression and endothelial barrier function. Revealing how integrin b1 acetylation regulates endothelial cell junctions offers new therapeutic possibilities for controlling vascular permeability.

2024-01-01 | GSE238019 | GEO

Cre-mediated deletion of b1 integrin in pancreatic b-cells

Project description:In this study, we investigated the function of beta integrins in developing islet beta-cells by targeting the deletion of exon 3 of the B1 integrin gene using a Cre-lox approach. Our results demonstrate that this class of integrin receptors is critically important for proper beta cell expansion during development

2013-07-31 | E-MEXP-3736 | biostudies-arrayexpress

Whole-genome gene expression profiles of non-tumorous human lung tissues: Laval set

Project description:We profiled genome-wide gene expression in non-tumorous human lung tissues. The overall goal of this project is to improve our molecular understanding of various lung diseases including lung cancer and chronic obstructive pulmonary disease (COPD). Lung specimens were obtained from patients undergoing lung cancer surgery at the Institut Universitaire de Cardiologie et de Pneumologie de Québec. All lung specimens were derived from a homogeneous piece of peripheral tissue free of tumour obtained at surgery performed between April 2004 and December 2008. These lung tissues were stored in the biobank of the Respiratory Health Network of the FRSQ, site Institut Universitaire de Cardiologie et de Pneumologie de Québec. The time from surgical removal to freezing was between 15 to 30 minutes. RNAs were extracted and then hybridized to a single custom-made whole-genome human Affymetrix array.

2012-06-10 | E-GEOD-23352 | biostudies-arrayexpress

Deciphering the mammary stem cell niche: a role for laminin-binding integrins

Project description:Integrin dimers a3/b1, a6/b1 and a6/b4 are the receptors of mammary epithelial cells for Laminin, major component of the mammary basement membrane. Antibodies against a6 and a3 integrin chains serve to isolate stem cell enriched populations from mammary epithelium, however, role of integrin dimers comprising these chains in the control of mammary stem cell activity are not known. To investigate the role of Laminin-binding integrins in the control of mammary stem cell function, a3 and a6 chains were deleted from mammary basal cells in vitro using Cre-recombinase carrying adenovirus. We found that deletion of single integrin chain (either a3, or a6) did not significantly affect stem cell potential as evaluated by transplantation and mammosphere assays, whereas basal cells depleted of both a3 and a6 integrin chains (a3a6KO) presented severely diminished stem cell activity. In this study the transcriptional profiles of a3a6KO were analysed and compared to those of control cells.

2019-04-23 | GSE117120 | GEO

Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

Project description:Increased myeloid-derived suppressor cell (MDSC) frequency is associated with worse outcomes and poor therapeutic response in multiple types of cancer. In the glioblastoma (GBM) microenvironment, monocytic (m) MDSCs represent the predominant subset. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared to granulocytic (g) MDSCs has yet to be determined. Here we performed first broad epigenetic profiling of MDSC subsets to define underlying cell-intrinsic differences in their behavior and found that mMDSCs and gMDSCs display differences in their tumor-accelerating ability, with mMDSCs driving tumor growth in GBM models. Epigenetic assessments revealed enhanced gene accessibility for cell adhesion programs in mMDSCs and higher integrin b1 expression and function in mouse and human mMDSCs. Integrin b1 blockage abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment. These findings suggest that integrin b1 expression underlies the enrichment of mMDSCs in tumors and represents a putative immunotherapy target to attenuate myeloid cell-driven immune suppression in GBM.

2022-06-26 | GSE206551 | GEO

The effect of aneuploidy on gene expression

2013-07-02 | GSE23729 | GEO