预约演示

更新于：2025-05-07

FN1 x CD29

更新于：2025-05-07

基本信息

关联

项与 FN1 x CD29 相关的药物

Fibronectin

靶点

CD29 x FN1

作用机制

CD29激动剂 [+1]

在研机构-

原研机构

JCR Pharmaceuticals Co., Ltd.

在研适应症-

非在研适应症

角膜疾病

最高研发阶段终止

首次获批国家/地区-

首次获批日期1800-01-20

项与 FN1 x CD29 相关的临床试验

JPRN-jRCTs061180037

/ Recruiting临床2期IIT

Clinical efficacy of the PHSRN peptide from fibronectin eye drops for intractable corneal epithelial disorders - Clinical efficacy of the PHSRN peptide from fibronectin eye drops for intractable corneal epithelial disorders

开始日期2009-03-27

申办/合作机构-

100 项与 FN1 x CD29 相关的临床结果

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100 项与 FN1 x CD29 相关的转化医学

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0 项与 FN1 x CD29 相关的专利（医药）

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1,030

项与 FN1 x CD29 相关的文献（医药）

2025-05-01·Journal of Proteomics

iTRAQ-based quantitative proteomics reveals dysregulation of fibronectin 1 contributes to impaired endometrial decidualization in recurrent implantation failure

Article

作者: Wu, Jiaqi ; Wang, Jingying ; Fang, Ying ; Zhao, Xuehan ; Yang, Xiaokui ; Wang, Cong ; Wang, Qin

Recurrent implantation failure (RIF) poses challenges to successful embryo implantation. In this study, we utilized isobaric tags for relative and absolute quantification (iTRAQ) to profile endometrial protein abundance in RIF patients. Through functional and pathway analyses, ECM-related proteins including fibronectin 1 (FN1), collagen type I alpha 2 chain (COL1A2), and integrin beta-1 (ITGB1) were revealed to be associated with RIF. Correlation analysis identified TGF-β1 as an upstream regulator of FN1. Knockdown experiments showed TGF-β1 downregulation could inhibit FN1 expression to inhibit decidualization markers. Our findings suggest a mechanistic link between TGF-β1/FN1 axis dysregulation and impaired decidualization observed in RIF. SIGNIFICANCE: Our study addresses the pressing issue of RIF, a significant obstacle in assisted reproductive technology. By employing isobaric tags for relative and absolute quantification (iTRAQ), we comprehensively analyzed endometrial protein abundance in RIF patients. Through functional and pathway enrichment analyses, we identified dysregulation in extracellular matrix (ECM)-related proteins, including FN1, COL1A2, and ITGB1, shedding light on their potential roles in implantation failure. Additionally, our correlation analysis revealed TGF-β1 as an upstream regulator of FN1, suggesting a novel regulatory axis involved in decidualization. Knockdown experiments further demonstrated the impact of TGF-β1 and FN1 on decidualization markers. This study contributes to a better understanding of the molecular mechanisms underlying RIF.

2025-03-20·Nan fang yi ke da xue xue bao = Journal of Southern Medical University

CEACAM6通过调控上皮间质转化抑制鼻咽癌细胞的增殖和迁移.

Article

作者: Wei, Zhuoli ; Xiang, Ping ; Tao, Lu ; Wang, Yueyue

目的: 明确CEACAM6在鼻咽癌中的表达，探索CEACAM6对鼻咽癌细胞增殖和迁移的影响以及潜在的作用机制。方法: 通过GEO数据库分析CEACAM6在鼻咽癌中表达情况。TCGA数据库分析CEACAM6在头颈部癌中表达情况以及与生存预期的关系。免疫组织化学技术检测CEACAM6在鼻咽癌组织中的表达情况。构建CEACAM6过表达细胞模型，分为control组（空载）和Lv-CEACAM6组（过表达）；CEACAM6敲低细胞模型，分为control组（空载）、sh#1组（敲低）和sh#2组（敲低）。通过CCK-8和Edu染色检测CEACAM6对鼻咽癌细胞增殖的影响。伤口愈合和Transwell检测CEACAM6对鼻咽癌细胞侵袭迁移的影响。鬼笔环肽染色检测CEACAM6对鼻咽癌细胞骨架排列的影响。Western blotting检测CEACAM6对鼻咽癌细胞中FN1、ITGA5、ITGB1、N-cad、Vim和E-cad的蛋白表达影响以及FN1过表达对CEACAM6过表达的鼻咽癌细胞中ITGA5和ITGB1蛋白表达的影响。结果: GEO数据库分析表明CEACAM6在鼻咽癌中低表达，TCGA数据库分析表明CEACAM6在头颈部癌中低表达，CEACAM6低表达与预后不良有关。免疫组织化学技术检测结果显示CEACAM6在鼻咽癌组织中低表达。CCK-8和Edu检测结果显示CEACAM6可抑制鼻咽癌细胞的增殖能力（P<0.05）。伤口愈合和Transwell检测结果显示CEACAM6可抑制鼻咽癌细胞侵袭和迁移能力（P<0.05）。鬼笔环肽染色结果显示上调CEACAM6表达后肌动蛋白荧光表达降低。Westen blotting检测结果表明上调CEACAM6表达后FN1、ITGA5、ITGB1下调，E-cad上调，N-cad和Vim下调（P<0.05），FN1过表达可缓解CEACAM6对ITGA5和ITGB1表达的抑制作用（P<0.05）。结论: CEACAM6可能通过调控FN1、ITGA5、ITGB1蛋白表达影响上皮间质转化从而抑制鼻咽癌的侵袭和迁移。.

2025-03-01·Journal of Biological Chemistry

Integrin beta 1 and fibronectin mediate extracellular vesicle uptake and functional RNA delivery

Article

作者: Elsharkasy, Omnia M ; Gitz-Francois, Jerney J ; Seinen, Cornelis W ; de Jong, Olivier G ; Schiffelers, Raymond M ; Vader, Pieter ; van der Werff, Leanne ; Tognoli, Maria Laura ; de Voogt, Willemijn S

Extracellular vesicles (EVs) are cell-derived vesicles secreted by all cell types into the extracellular spaces. EVs comprise a heterogenous population of vesicles that carry bioactive molecules, such as proteins, lipids, and RNAs, which they can deliver to recipient cells. Over the past few years, EVs have been recognized for their vital role in intercellular communication, and thereby in various physiological and pathological processes. In addition, EVs are increasingly being studied as potential drug delivery vehicles. It is therefore crucial to understand the mechanisms and molecular players underlying EV uptake and functional cargo delivery. Several studies have investigated various EV uptake pathways; nonetheless, molecular mechanisms governing uptake and cargo transfer remain largely lacking. Here, we show, using a CRISPR/Cas9-mediated reporter system, that integrin β1 on recipient cells plays an important role in EV uptake and EV-mediated RNA delivery. Additionally, using both RNA interference and blocking antibodies, we show that association of integrin β1 with integrin α4 is essential for this process. We demonstrate that α4β1 on recipient cells interacts with EVs through surface localized fibronectin via binding to its leucine-aspartic acid-valine motif, and that blocking of this interaction reduces both EV uptake and RNA delivery. Thus, we identify a key mechanism in EV uptake and cargo delivery which could potentially facilitate research into EV biology and pave the way for the development of novel therapeutic approaches by targeting pathways that lead to functional cargo delivery.

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