FILIP1L

Last update 08 May 2025

Basic Info

Synonyms

130 kDa GPBP-interacting protein, 90 kDa GPBP-interacting protein, COL4A3BPIP

+ [8]

Introduction

Acts as a regulator of the antiangiogenic activity on endothelial cells. When overexpressed in endothelial cells, leads to inhibition of cell proliferation and migration and an increase in apoptosis. Inhibits melanoma growth When expressed in tumor-associated vasculature.

100 Clinical Results associated with FILIP1L

100 Translational Medicine associated with FILIP1L

0 Patents (Medical) associated with FILIP1L

Literatures (Medical) associated with FILIP1L

01 Jan 2025·microPublication biology

Filamin A interacting protein 1-like (FILIP1L) has mitochondrial localization.

Article

Author: Odell, Jacob ; Lammerding, Jan ; Bockley, Karisa ; Henretta, Sarah

Filamin A interacting protein 1-like (FILIP1L) is a multifunctional protein that plays a role in cancer progression, apoptosis, and angiogenesis. However, FILIP1L remains a relatively underexplored protein, and many of FILIP1L's key mechanisms and interacting partners are still unknown. Using immunofluorescence staining for endogenous FILIP1L and high-resolution confocal microscopy, we show that FILIP1L colocalizes with the mitochondrial marker, TOM20, suggesting a novel connection between FILIP1L and mitochondria. Further exploring the relationship between FILIP1L and mitochondria might provide a deeper understanding of the emerging function of FILIP1L in health and disease.

01 Oct 2024·Current Medical Science

Key Genes Involved in the Beneficial Mechanism of Hyperbaric Oxygen for Glioblastoma and Predictive Indicators of Hyperbaric Oxygen Prolonging Survival in Glioblastoma Patients

Article

Author: Ren, Zi-Qi ; Li, Dong-Guo ; Yu, Qiu-Hong ; Wang, Cong ; Liu, Ya-Ling ; Ren, Xiao-Hui ; Wang, Ren-Dong

OBJECTIVEThe prognosis of glioblastoma is poor, and therapy-resistance is largely attributed to intratumor hypoxia. Hyperbaric oxygen (HBO) effectively alleviates hypoxia. However, the sole role of HBO in glioblastoma remains controversial. We previously reported that HBO can promote apoptosis, shorten protrusions, and delay growth of glioblastoma, but the molecular mechanism is unclear. We aimed to test candidate genes in HBO-exposed glioblastoma cells and to analyze their correlation with the survival of glioblastoma patients.METHODSGlioblastoma cell lines exposed to repetitive HBO or normobaric air (NBA) were collected for RNA isolation and microarray data analysis. GO analysis, KEGG pathway analysis and survival analysis of the differentially expressed genes (DEGs) were performed.RESULTSHBO not only inhibited hypoxia-inducing genes including CA9, FGF11, PPFIA4, TCAF2 and SLC2A12, but also regulated vascularization by downregulating the expression of COL1A1, COL8A1, COL12A1, RHOJ and FILIP1L, ultimately attenuated hypoxic microenvironment of glioblastoma. HBO attenuated inflammatory microenvironment by reducing the expression of NLRP2, CARD8, MYD88 and CD180. HBO prevented metastasis by downregulating the expression of NTM, CXCL12, CXCL13, CXCR4, CXCR5, CDC42, IGFBP3, IGFBP5, GPC6, MMP19, ADAMTS1, EFEMP1, PTBP3, NF1 and PDCD1. HBO upregulated the expression of BAK1, PPIF, DDIT3, TP53I11 and FAS, whereas downregulated the expression of MDM4 and SIVA1, thus promoting apoptosis. HBO upregulated the expression of CDC25A, MCM2, PCNA, RFC33, DSCC1 and CDC14A, whereas downregulated the expression of ASNS, CDK6, CDKN1B, PTBP3 and MAD2L1, thus inhibiting cell cycle progression. Among these DEGs, 17 indicator-genes of HBO prolonging survival were detected.CONCLUSIONSHBO is beneficial for glioblastoma. Glioblastoma patients with these predictive indicators may prolong survival with HBO therapy. These potential therapeutic targets especially COL1A1, ADAMTS1 and PTBP3 deserve further validation.

01 May 2024·Biochemical Pharmacology

TDO2 promotes bladder cancer progression via AhR-mediated SPARC/FILIP1L signaling

Article

Author: Yin, Lei ; Shi, Xiaokai ; Gao, Shenglin ; Jin, Yunjie ; Ding, Xiaoju ; Jin, Zhibo ; Wang, Yidi ; Yang, Jinjian ; Lei, Yibo

The enzyme tryptophan 2,3-dioxygenase (TDO2) has been implicated in the dysregulation across a variety of human cancers. Despite this association, the implications of TDO2 in the progression of bladder cancer have eluded thorough understanding. In this study, we demonstrate that TDO2 expression is notably elevated in bladder cancer tissues and serves as an unfavorable prognostic factor for overall survival. Through a series of biological functional assays, we have determined that TDO2 essentially enhances cell proliferation, metastatic potential, and imparts a decreased sensitivity to the chemotherapeutic agent cisplatin. Our mechanistic investigations reveal that TDO2 augments aryl hydrocarbon receptor (AhR) signaling pathways and subsequently upregulates the expression of SPARC and FILIP1L. Importantly, we have identified a positive correlation between TDO2 levels and the basal/squamous subtype of bladder cancer, and we provide evidence to suggest that TDO2 expression is modulated by the tumor suppressors RB1 and TP53. From a therapeutic perspective, we demonstrate that the targeted inhibition of TDO2 with the molecular inhibitor 680C91 markedly attenuates tumor growth and metastasis while concurrently enhancing the efficacy of cisplatin. These findings open a new therapeutic avenue for the management of bladder cancer.

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FILIP1L

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