Non-integrin laminin receptors in epithelia

Cloutier, Gabriel; Sallenbach-Morrissette, Amélie; Beaulieu, Jean‐François

doi:10.1016/j.tice.2018.12.005

Cited by 22 publications

(24 citation statements)

References 90 publications

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“…The 67LR is the first non-integrin laminin receptor identified by binding to immobilized laminin-1 [ 19 ]. 67LR is involved in cell proliferation, protein synthesis, cell survival, cell adhesion, and migration [ 20 ]. In addition, 67LR stabilizes or modulates the binding of laminin to other receptors [ 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Blockade of 67-kDa Laminin Receptor Facilitates AQP4 Down-Regulation and BBB Disruption via ERK1/2-and p38 MAPK-Mediated PI3K/AKT Activations

Kim

Park

Lee

et al. 2020

Cells

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Recently, we have reported that dysfunctions of 67-kDa laminin receptor (67LR) induced by status epilepticus (SE, a prolonged seizure activity) and 67LR neutralization are involved in vasogenic edema formation, accompanied by the reduced aquaporin 4 (AQP4, an astroglial specific water channel) expression in the rat piriform cortex (PC). In the present study, we found that the blockade of 67LR activated p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways, which enhanced phosphatidylinositol 3 kinase (PI3K)/AKT phosphorylations in endothelial cells and astrocytes, respectively. 67LR-p38 MAPK-PI3K-AKT activation in endothelial cells increased vascular permeability. In contrast, 67LR-ERK1/2-PI3K-AKT signaling pathways in astrocytes regulated astroglial viability and AQP4 expression. These findings indicate that PI3K/AKT may integrate p38 MAPK and ERK1/2 signaling pathways to regulate AQP4 expression when 67LR functionality is reduced. Thus, we suggest that 67LR-p38 MAPK/ERK1/2-PI3K-AKT-AQP4 signaling cascades may mediate serum extravasation and AQP4 expression in astroglio-vascular systems, which is one of the considerable therapeutic targets for vasogenic edema in various neurological diseases.

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Section: Introductionmentioning

confidence: 99%

Blockade of 67-kDa Laminin Receptor Facilitates AQP4 Down-Regulation and BBB Disruption via ERK1/2-and p38 MAPK-Mediated PI3K/AKT Activations

Kim

Park

Lee

et al. 2020

Cells

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“…Cell adhesion is mediated by membrane receptors specific for these glycoproteins. In the intestine, there are a number of these receptors that have been identified for epithelial cells including dystroglycan and the 37/67 kDa laminin receptor [1] as well as many that belong to the integrin family [2,3]. Integrins are transmembrane αβ heterodimers that function as bidirectional signal transduction mediators acting as mechanosensors and participating in the regulation of main cell functions such as adhesion, migration, proliferation, survival and differentiation [4,5].…”

Section: Introductionmentioning

confidence: 99%

Integrin α6β4 in Colorectal Cancer: Expression, Regulation, Functional Alterations and Use as a Biomarker

Beaulieu

2019

Cancers

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Integrin α6β4 is one of the main laminin receptors and is primarily expressed by epithelial cells as an active component of hemidesmosomes. In this article, after a brief summary about integrins in the gut epithelium in general, I review the knowledge and clinical potential of this receptor in human colorectal cancer (CRC) cells. Most CRC cells overexpress both α6 and β4 subunits, in situ in primary tumours as well as in established CRC cell lines. The mechanisms that lead to overexpression have not yet been elucidated but clearly involve specific transcription factors such as MYC. From a functional point of view, one key element affecting CRC cell behaviour is the relocalization of α6β4 to the actin cytoskeleton, favouring a more migratory and anoikis-resistant phenotype. Another major element is its expression under various molecular forms that have the distinct ability to interact with ligands (α6β4 ± ctd) or to promote pro- or anti-proliferative properties (α6Aβ4 vs. α6Bβ4). The integrin α6β4 is thus involved in most steps susceptible to participation with CRC progression. The potential clinical significance of this integrin has begun to be investigated and recent studies have shown that ITGA6 and ITGB4 can be useful biomarkers for CRC early detection in a non-invasive assay and as a prognostic factor, respectively.

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“…In addition, MET promotes cell motility may also contribute GC development (32). Nonintegrin membrane-ECM interactions, such as dystroglycan and 37/67 laminin receptor, is found to be related to variety of epithelial cancers (33).…”

Section: Discussionmentioning

confidence: 99%

Identification of lncRNA-associated competing endogenous RNA networks for occurrence and prognosis of gastric carcinoma

Jin

2020

Preprint

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Background: Gastric cancer (GC) is one of the common digestive malignancies worldwide and causes a severe public health issue. So far, the underlying mechanisms of GC are largely unclear. Thus, our aim is to identify the long non-coding RNA (lncRNA) associated competing endogenous RNA (ceRNA) specialized for occurrence and progression in GC.Methods: The comprehensive online dataset, TCGA, was downloaded and used for identification of differentially expressed (DE) lncRNA, miRNA and mRNA screen with the value of logFC = 1 and FDR < 0.05, respectively. The interactions between lncRNA and miRNA as well mRNA and miRNA were predicted via multiple online databases, such as miRcode and Targetscan. Then the ceRNA network was constructed accompanied with gene set enrichment analysis and survival analysis. In addition, RT-qPCR and in vitro assay was carried out to validate the effect of the hub lncRNAs.Results: We identified 1485 lncRNAs, 312 miRNAs and 4260 mRNAs were differentially expressed between GC and normal tissues, respectively. Then, we generated a ceRNA network with 909 edges and 253 nodes including 76 lncRNA, 18 miRNA and 159 mRNA. This ceRNA network was involved in MET activates PTK2 signalling, MET promotes cell motility and non-integrin membrane-ECM interactions. Next, by univariate and multivariate analysis, there were 9 hub lncRNAs emerged and were associated subnetwork involved in actin filament binding and MAPK signaling pathway. The in vitro assay indicated lncRNA INHBA-AS1 and CCDC144NL-AS1 may positively related to the GC aggressive features, including proliferation, invasion and migration.Conclusion: In summary, we constructed a ceRNA network involved in the GC development. Moreover, we also identified 9 hub lncRNA-associated network related to prognosis of GC and validated two out of them as promising oncogenes. This may provide potential biomarkers or therapeutic target for GC in future.

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Non-integrin laminin receptors in epithelia

Cited by 22 publications

References 90 publications

Blockade of 67-kDa Laminin Receptor Facilitates AQP4 Down-Regulation and BBB Disruption via ERK1/2-and p38 MAPK-Mediated PI3K/AKT Activations

Blockade of 67-kDa Laminin Receptor Facilitates AQP4 Down-Regulation and BBB Disruption via ERK1/2-and p38 MAPK-Mediated PI3K/AKT Activations

Integrin α6β4 in Colorectal Cancer: Expression, Regulation, Functional Alterations and Use as a Biomarker

Identification of lncRNA-associated competing endogenous RNA networks for occurrence and prognosis of gastric carcinoma

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