Request Demo

Last update 08 May 2025

EDIL3

Last update 08 May 2025

Basic Info

Synonyms

DEL1, Developmentally-regulated endothelial cell locus 1 protein, EDIL3

+ [3]

Introduction

Promotes adhesion of endothelial cells through interaction with the alpha-v/beta-3 integrin receptor. Inhibits formation of vascular-like structures. May be involved in regulation of vascular morphogenesis of remodeling in embryonic development.

Drugs associated with EDIL3

WO2024120484

Patent Mining

Target

EDIL3

Mechanism-

Active Org.

Nona Biosciences Suzhou Co. Ltd. [+1]

Originator Org.

Nona Biosciences Suzhou Co. Ltd. [+1]

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with EDIL3

100 Translational Medicine associated with EDIL3

0 Patents (Medical) associated with EDIL3

277

Literatures (Medical) associated with EDIL3

01 Aug 2025·International Journal of Cardiology

DEL-1 promotes macrophage lipid accumulation and inflammation by inhibiting TGF-β

Letter

Author: Liu, Xian ; Wang, Yu-Ping ; Zhu, Lin ; Sun, Shao-Yang ; Ren, Kun

01 Apr 2025·Gene

Developmental endothelial locus-1 as a potential biomarker for the formation and progression of intracranial aneurysm

Article

Author: Li, Jiaoxing ; Lan, Kai ; Xie, Yi ; Chen, Jie ; Ye, Fei ; Zhang, Minghao ; Wu, Xiaoxin ; Sheng, Wenli

BACKGROUNDIntracranial aneurysms (IAs) are pathological dilations occurring at major branch points of cerebral arteries, which can lead to aneurysmal subarachnoid hemorrhage (aSAH) upon rupture. Recent studies have identified developmental endothelial locus-1 (DEL1) as closely associated with IA, though its role remains not fully understood. This study aimed to investigate serum DEL1 level differences in IA patients and explore its function in vascular endothelial cells.METHODSWe enrolled 32 IA patients and 32 healthy controls at our hospital between February 2024 and August 2024. Clinical data were collected from electronic medical records. Peripheral blood samples were taken preoperatively to measure serum DEL1 concentrations using enzyme-linked immunosorbent assay (ELISA). Functional assays were conducted on human umbilical vein endothelial cells (HUVECs) in vitro.RESULTSSerum DEL1 levels were significantly lower in IA patients compared to healthy controls. Subgroup analysis showed that DEL1 levels were lower in patients with ruptured IAs and multiple IAs. Serum DEL1 level exhibits good performance as a biomarker for IA and aSHA. Additionally, in vitro experiments demonstrated that DEL1 knockdown (siDEL1) in HUVECs significantly enhanced cell proliferation, migration, and tube formation, while abnormal shear stress reduced endothelial DEL1 gene expression and disrupted endothelial barrier, suggesting a role in IA formation and progression.CONCLUSIONOur findings suggest that decreased serum DEL1 levels may serve as a potential biomarker for the formation and progression of IAs. DEL1 could be a key target for future studies investigating the pathogenesis of IA and aSAH.

01 Dec 2024·Molecular Biology Reports

Nischarin inhibits the epithelial-mesenchymal transition process and angiogenesis in breast cancer cells by inactivating FAK/ERK signaling pathway via EGF like repeats and discoidin domains 3

Article

Author: He, Yibo ; Xie, Shangnao ; Chen, Yidan ; Yang, Lingrong ; Zheng, Ruzhen ; Wang, Rui

BACKGROUNDOur previous study has demonstrated that Nischarin (NISCH) exerts its antitumor effects in breast cancer (BC) by suppressing cell migration and invasion. This study aims to explore the underlying mechanism through which NISCH functions in BC.METHODS AND RESULTSThe relevance between EGF Like Repeats and Discoidin Domains 3 (EDIL3) mRNA expression and the overall survival of tumor patients was depicted by the Kaplan-Meier curve. The findings revealed that overexpressed NISCH attenuated cell motility and colony-forming capacities of Hs578T cells, yet silenced NISCH in MDA-MB-231 cells led to contrasting results. Western blot (WB) analysis indicated that overexpression of NISCH significantly down-regulated the Vimentin and Slug expression, and inactivated the FAK/ERK signaling pathway. RNA sequencing (RNA-seq) was performed in NISCH-overexpressed Hs578T cells and the control cells to analyze differentially expressed genes (DeGs), and the results showed a significant down-regulation of EDIL3 mRNA level upon overexpression of NISCH. Subsequent functional analyses demonstrated that overexpression of EDIL3 attenuated the inhibitory effect of NISCH on cell migration, invasion, colony formation, and tube formation.CONCLUSIONIn summary, our finding preliminarily revealed that NISCH inhibits the epithelial-mesenchymal transition (EMT) process and angiogenesis in BC cells by down-regulating EDIL3 to inactivate the FAK/ERK signaling pathway, thereby suppressing the progression of BC. Our results hold promise for contributing to the deep understanding of BC pathogenesis and identifying new therapeutic strategies for clinical application.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

EDIL3

Basic Info

Related

Analysis