Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lysyl oxidase-like 2 (LOXL2) a new regulator of cell polarity required for metastatic dissemination of basal-like breast carcinomas

ABSTRACT: Basal-like breast carcinoma is characterized by the expression of basal/myoepithelial markers, undifferentiated phenotype, highly aggressive behaviour and a frequent triple negative status (ESR-, PR-, Her2neu-). We have previously shown that epithelial-mesenchymal transition (EMT) occurs in basal-like breast tumours and identified Lysyl- Oxidase-Like 2 (LOXL2) as an EMT player and a poor prognosis marker in squamous cell carcinomas. We now show that LOXL2 mRNA is overexpressed in basal-like human breast carcinomas. Identification of new molecular markers in basal breast carcinomas

ORGANISM(S): Homo sapiens

PROVIDER: GSE29581 | GEO | 2011/10/21

SECONDARY ACCESSION(S): PRJNA141413

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Lysyl oxidase-like 2 (LOXL2) a new regulator of cell polarity required for metastatic dissemination of basal-like breast carcinomas

Project description:Basal-like breast carcinoma is characterized by the expression of basal/myoepithelial markers, undifferentiated phenotype, highly aggressive behaviour and a frequent triple negative status (ESR-, PR-, Her2neu-). We have previously shown that epithelial-mesenchymal transition (EMT) occurs in basal-like breast tumours and identified Lysyl- Oxidase-Like 2 (LOXL2) as an EMT player and a poor prognosis marker in squamous cell carcinomas. We now show that LOXL2 mRNA is overexpressed in basal-like human breast carcinomas. Identification of new molecular markers in basal breast carcinomas 58 (IDC) infiltrative breast ductal carcinoma samples (Grade 3)

2011-10-20 | E-GEOD-29581 | biostudies-arrayexpress

LOXL2 drives epithelial-mesenchymal transition via activation of IRE1-XBP1 branch of unfolded protein response.

Project description:Epithelial-to-Mesenchymal Transition (EMT) is a key process contributing to the aggressiveness of cancer cells. EMT is triggered by activation of different transcription factors collectively known as EMT-TFs. Different cellular cues and cell signalling networks activate EMT at transcriptional and posttranscriptional level in different biological and pathological situations. Among them, overexpression of LOXL2 (lysyl oxidase-like 2) induces EMT independent of its catalytic activity. Remarkably, perinuclear/cytoplasmic accumulation of LOXL2 is a poor prognosis marker of squamous cell carcinomas and is associated to basal breast cancer metastasis by mechanisms no yet fully understood. Here, we report that overexpression of LOXL2 promotes its accumulation in the Endoplasmic Reticulum where it interacts with HSPA5 leading to activation of the IRE1-XBP1-branch of the Unfolded Protein Response (UPR). LOXL2-dependent UPR activation induces the expression of several EMT-TFs: SNAI1, SNAI2, ZEB2 and TCF3 that are direct transcriptional targets of XBP1. Remarkably, inhibition of IRE1 blocks LOXL2-dependent upregulation of EMT-TFs thus hindering EMT induction. LOXL2 relationship to Endoplasmic Reticulum Stress

2017-05-11 | GSE90605 | GEO

Exogenous expression of Lox, Loxl1 and Loxl2 regulate gene expression in primary murine lung fibroblasts.

Project description:Primary murine lung fibroblasts were transfected with either control (scrambled) or sequence-specific siRNA against Lysyl oxidase (Lox), Lysyl oxidase-like (Loxl1) or Lysyl oxidase-like 2 (Loxl2) genes. Cells were harvested 48 hours after the transfection. Multiple changes in gene expression were found in the corrected p values in this microarray study.

2016-10-25 | GSE89121 | GEO

A novel Lysyl oxidase like 2 alternative splicing LOXL2 â³e13 in esophageal squamous carcinoma cells

Project description:A novel alternative splicing isoform of LOXL2 â³e13 was expressed ubiquitously in all cell lines and ESCC tissues. In contrast to the impaired deamination enzymatic activity compared with full length LOXL2, LOXL2 â³e13 showed an enhanced ability to promote cell mobility and invasiveness in ESCC cells than full length LOXL2 through a different mechanism. We used cDNA microarrays to identify genes that were differentially expressed upon LOXL2 â³ e13 overexpressed. For this purpose, we selected LOXL2 â³ e13, WT and empty vector control transfeced ESCC KYSE150 cell lines. Total RNA was extracted,compare the gene expression patterns between LOXL2 â³e13, LOXL2 WT and empty vector control transfected cells through the Genechip Primeview Human Gene Expression Array.

2016-07-03 | E-GEOD-53676 | biostudies-arrayexpress

Expression data in human esophageal squamous carcinoma cell line KYSE150 with LOXL2 delta 72 over-expression

Project description:We have identified a new novel spliced variant of Lysyl Oxidase-like 2 (LOXL2), termed LOXL2 delta72, in human oesophageal carcinoma cells (ESCC). To explore the biological function of this variant, the cDNA microarrays was perform to assess the genes expression induced by its over-expression in ESCC KYSE150. We used microarrays to detail the global programmed of genes expression when LOXL2 delta72 over-expressed in KYSE150 cells compared with wild-type LOXL2.

2016-03-28 | GSE53645 | GEO

A novel Lysyl oxidase like 2 alternative splicing LOXL2 △e13 in esophageal squamous carcinoma cells

Project description:A novel alternative splicing isoform of LOXL2 △e13 was expressed ubiquitously in all cell lines and ESCC tissues. In contrast to the impaired deamination enzymatic activity compared with full length LOXL2, LOXL2 △e13 showed an enhanced ability to promote cell mobility and invasiveness in ESCC cells than full length LOXL2 through a different mechanism.

2016-01-01 | GSE53676 | GEO

LOXL2-mediated chromatin compaction is required to maintain the oncogenic properties of triple-negative breast cancer cells

Project description:Oxidation of histone H3 at lysine 4 (H3K4ox) is catalyzed by lysyl oxidase–like 2 (LOXL2). This histone modification is enriched in heterochromatin in triple-negative breast cancer (TNBC) cells and has been linked to the maintenance of compacted chromatin. However, the molecular mechanism underlying this maintenance is still unknown. Here we show that LOXL2 interacts with RUVBL1, RUVBL2, BAF53, and DMAP1, a complex involved in the incorporation of the histone variant H2A.Z. Our experiments indicate that this interaction and the active form of RUVBL2 are required to maintain LOXL2-dependent chromatin compaction. Genome-wide experiments showed that H2A.Z, RUVBL2, and H3K4ox colocalize in heterochromatin regions. In the absence of LOXL2 or RUVBL2, global levels of the heterochromatin histone mark H3K9me3 were strongly reduced, and the ATAC-seq signal in the H3K9me3 regions was increased. Finally, we observed that the interplay between these series of events is required to maintain H3K4ox-enriched heterochromatin regions, which in turn is key for maintaining the oncogenic properties of the TNBC cell line tested (MDA-MB-231).

2023-12-31 | GSE142463 | GEO

Spatial transcriptomic validation of a biomimetic model of fibrosis enables re-evaluation of a therapeutic antibody targeting LOXL2

Project description:Matrix stiffening by lysyl oxidase-like 2 (LOXL2) mediated collagen cross-linking is proposed as a core feed-forward mechanism that promotes fibrogenesis. Failure in clinical trials of simtuzumab (the humanized version of AB0023, a monoclonal antibody against human LOXL2) suggested targeting LOXL2 may not have disease relevance, however target engagement was not directly evaluated. We compared the spatial transcriptome of active human lung fibrogenesis sites with different human cell culture models to determine the model with greatest disease relevance. Within the selected model system, we then evaluated AB0023, identifying that it did not inhibit collagen cross-linking or reduce tissue stiffness, nor did it inhibit LOXL2 catalytic activity. In contrast it did potently inhibit angiogenesis consistent with an alternative, non-enzymatic mechanism of action. Thus, AB0023 is anti-angiogenic but does not inhibit LOXL2 catalytic activity, collagen cross-linking or tissue stiffening. These findings have implications for the interpretation of lack of efficacy of simtuzumab in clinical trials of fibrotic diseases.

2024-02-19 | GSE255705 | GEO

Microarray of lysyl oxidase-like 2 (LOXL2)-overexpressing human buccal SCC TW2.6 and hypopharyngeal SCC FaDu cells against respective vector controls

Project description:To investigated the effects of LOXL2 overexpression in HNSCC TW2.6/FaDu cells. 8 samples

2022-04-22 | GSE201040 | GEO

Homo sapiens

Project description:Lysyl oxidase-like 2 (LOXL2) a new regulator of cell polarity required for metastatic dissemination of basal-like breast carcinomas

| PRJNA141413 | ENA

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