FERMT1

Last update 08 May 2025

Basic Info

Synonyms

C20orf42, FERM domain containing kindlin 1, Fermitin family homolog 1

+ [9]

Introduction

Involved in cell adhesion. Contributes to integrin activation. When coexpressed with talin, potentiates activation of ITGA2B. Required for normal keratinocyte proliferation. Required for normal polarization of basal keratinocytes in skin, and for normal cell shape. Required for normal adhesion of keratinocytes to fibronectin and laminin, and for normal keratinocyte migration to wound sites. May mediate TGF-beta 1 signaling in tumor progression.

100 Clinical Results associated with FERMT1

100 Translational Medicine associated with FERMT1

0 Patents (Medical) associated with FERMT1

250

Literatures (Medical) associated with FERMT1

01 May 2025·Gastric Cancer

FERMT2 drives anoikis resistance and peritoneal metastasis by enhancing extracellular matrix deposition in gastric cancer

Article

Author: Zhu, Songting ; Wang, Haiyong ; Yang, Yan ; Zhou, Zheng ; Teng, Lisong ; He, Chao

AbstractPeritoneal metastasis is a critical step in the progression of gastric cancer (GC), yet its underlying mechanisms remain poorly understood. Here, we identify FERMT2, a member of the Kindlin protein family, as a key regulator of anoikis resistance (AR) and peritoneal metastasis in GC. FERMT2 expression increases in a suspension-time-dependent manner and is associated with higher pathological grade, advanced clinical stage, and poorer prognosis. Functional studies in vitro and in vivo demonstrate that FERMT2 promotes AR and facilitates peritoneal metastasis. Mechanistically, FERMT2 suppresses the ubiquitination of SOX2, thereby enhancing its stability and up-regulating FN1 transcription. Furthermore, we report that TGFβ-RI expression also increases in a suspension-time-dependent manner, forming a positive feedback loop with FERMT2 via TGFβ-1/TGFβ-RI signaling. This feedback loop drives extracellular fibronectin matrix deposition, strengthens cell–matrix interactions, and supports AR. These findings establish FERMT2 as a pivotal mediator of peritoneal metastasis in GC, offering insights into its potential as a therapeutic target.

01 Apr 2025·Biomedicine & Pharmacotherapy

Mineralocorticoid receptor antagonism improves corneal integrity in a rat model of limbal stem cell deficiency

Article

Author: Bonnet, Clémence ; Yesilirmak, Nilufer ; Gélizé, Emmanuelle ; Jonet, Laurent ; Bourges, Jean-Louis ; Zhu, Linxin ; Behar-Cohen, Francine ; Rodrigues-Braz, Daniela ; Jaisser, Frédéric ; Zhao, Min

Limbal stem cell deficiency (LSCD) is a sight-threatening condition caused by the loss and/or dysfunction of limbal stem cells (LSCs), which are essential for corneal epithelial regeneration and homeostasis and are critical for maintaining corneal transparency. We have previously shown that specific inactivation of the endothelial mineralocorticoid receptor (MR) inhibits corneal neovascularization (CN) and that MR antagonists (MRA) improve corneal epithelial wound healing. This study investigated the therapeutic potential of MRA in LSCD and their mechanisms of action. Using a rat model of LSCD, systemic administration of spironolactone (SPL) or a more specific MRA, eplerenone, similarly reduced CN and corneal oedema, demonstrating MR-specific effects. SPL further limited inflammation, enhanced the corneal epithelial barrier, reduced corneal conjunctivalization and promoted nerve regeneration, highlighting its potential to improve corneal integrity. Transcriptomic analysis revealed that SPL upregulated genes associated with LSC maintenance (Tp63, Wnt6), corneal epithelial differentiation (Vdr, Fermt1, Ehf) and nerve regeneration (Sprr1a, Anxa1), while downregulating genes associated with angiogenesis (Kdr, Scube2), inflammation (Ccl2, Cxcl1) and fibrosis (Fbln1, Snai1). Conversely, transgenic rats overexpressing human NR3C2 encoding MR showed corneal epithelial irregularities and dysregulation of genes related to extracellular matrix remodeling and fibrosis (Matn3, Serpine2, Fmod, Bgn, Ddr2), angiogenesis (Nrp2, Scube1) and limbal cell function (Ifitm3). These findings demonstrate that activation of the MR pathway disrupts limbal and corneal homeostasis and that SPL effectively modulates critical mechanisms in LSCD, offering promising therapeutic potential to reduce CN and improve corneal epithelial barrier integrity.

01 Dec 2024·International Immunopharmacology

FERMT1 contributes to the epithelial-mesenchymal transition of chronic rhinosinusitis with nasal polyps via PI3K/Akt signaling

Article

Author: Tang, Wenrui ; Chen, Han ; Han, Lin ; Dong, Zihui ; Zheng, Chunge ; Wang, Lin ; Jiang, Yan ; Zhang, Jisheng ; Yu, Longgang ; Yan, Xudong

BACKGROUNDEpithelial-mesenchymal transition (EMT) is a key process of chronic rhinosinusitis with nasal polyps (CRSwNP). The molecular mechanism of EMT in CRSwNP remains unknown. In this study, we aimed to investigate the role of FERMT1 during the EMT process in CRSwNP.METHODSWestern blotting, qRT-PCR, and immunohistochemistry (IHC) were performed to examine the expression of related proteins and mRNAs. The migration ability of human nasal epithelial cells (HNEpCs) was evaluated with wound scratch assay. RNA sequencing was performed to investigate the downstream genes of FERMT1. The CRSwNP mouse model was established to study the effect of FERMT1 in vivo.RESULTSWe found that FERMT1 was increased in nasal polyp tissues and correlated with the symptom scores of CRSwNP patients. Knockdown of FERMT1 inhibited the EMT process and cell migration induced by TGF-β1 through the PI3K/Akt pathway, and Akt inhibitor partially blocked the EMT induced by FERMT1 overexpression. In the CRSwNP mouse model, FERMT1 knockdown reduced nasal polyp formation and reversed the EMT process.CONCLUSIONSOur data indicate that knockdown of FERMT1 inhibits migration and EMT process of HNEpCs via PI3K/Akt signaling pathway, suggesting that FERMT1 may be a novel and potential therapeutic target for CRSwNP treatment.

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

FERMT1

Basic Info

Related

Analysis